shotha#dg11 gdg
DESCRIPTION
“PRELIMINARY PHYTOCHEMICAL INVESTIGATION & SHOTHAHARA (ANTI-INFLAMMATORY) EFFECT OF DEVADARU (CEDRUS DEODARA) ON ALBINO RATS AN EXPERIMENTAL STUDY ” - Dr. Shivaleela M.Kudari, Department of Dravya Guna, Post Graduate Studies & Research Centre, D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE,GADAGTRANSCRIPT
“PRELIMINARY PHYTOCHEMICAL INVESTIGATION
& SHOTHAHARA (ANTI-INFLAMMATORY) EFFECT
OF DEVADARU (CEDRUS DEODARA) ON ALBINO
RATS AN EXPERIMENTAL STUDY ”. BY
DDrr.. SShhiivvaalleeeellaa MM..KKuuddaarrii
Dissertation submitted to the Rajiv Gandhi University
of Health Sciences, Karnataka, Bangalore.
In partial fulfillment of Regulations for award of degree of
AAYYUURRVVEEDDAA VVAACCHHAASSPPAATTII MM..DD..
IN
DRAVYAGUNA
Under the guidance of
DR. KUBER. SANKH. M.D. (AYU)
DEPARTMENT OF DRAVYA GUNA
POST GRADUATE STUDIES & RESEARCH CENTER
SHRI D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG-582103
2007
DECLARATION BY THE CANDIDATE
I hereby declare that this dissertation / thesis entitled “Preliminary Phitochemical
investigation & Shothara (anti-inflammatory) effect of devadaru
(cedrusdeodara) on Albino rats – an Experimental study is a bonafide and genuine
research work carried out by me under the guidance of Dr. Kuber Sankh. MD (Ayu),
Asst. Professor, Department of Dravyaguna, Shri D.G.M.A.M.C, PGS & RC, Gadag.
Date: Signature of the Candidate
PLACE: (DDrr.. SShhiivvaalleeeellaa MM..KKuuddaarrii))
D.G.M.AYURVEDIC MEDICAL COLLEGE
POST GRADUATE STUDIES AND RESEARCH CENTRE
GADAG, 582 103
This is to certify that the dissertation entitled “Preliminary Phitochemical
investigation & Shothara (anti-inflammatory) effect of devadaru
(cedrusdeodara) on Albino rats – an Experimental study is a bonafide research
work done by Shivaleela. M. Kudari in partial fulfillment of the requirement for the
post graduation degree of “Ayurveda Vachaspati M.D. (Dravya Guna)” Under
Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka.
Guide Dr. KUBER SANKH
M.D. (Ayu) Asst. Professor
Dept of Dravya Guna
DGMAMC, PGS&RC, GADAG
Date:
Place: Gadag
J.S.V.V. SAMSTHE’S
D.G.M.AYURVEDIC MEDICAL COLLEGE
POST GRADUATE STUDIES AND RESEARCH CENTRE
GADAG, 582 103
Endorsement by the H.O.D,Principal/head of the
Institution
This is to certify that the dissertation entitled “Preliminary Phitochemical
investigation & Shothara (anti-inflammatory) effect of devadaru
(cedrusdeodara) on Albino rats - an Experimental study is a bonafide research
work done by Dr. Shivaleela M. Kudari under the guidance of
Dr. KUBER SANKH MD (Ayu), Asst. Professor, Department of Dravyaguna, in partial
fulfillment of the requirement for the post graduation degree of “Ayurveda
Vachaspati M.D. (Dravya Guna)” Under Rajiv Gandhi University of Health
Sciences, Bangalore, Karnataka.
(Dr. G.V. MULAGUND) (Dr. G.B. PATIL) Professor & H.O.D. Principal Dept of Dravya Guna DGM Ayurvedic Medical College, DGMAMC, PGS&RC. Gadag
Date: Date: Place: Gadag Place: Gadag
© Copy right
Declaration by the Candidate
I here by declare that the Rajiv Gandhi University of Health Sciences,
Karnataka shall have the rights to preserve, use and disseminate this dissertation /
thesis in print or electronic format for academic / research purpose.
Date:
Place: (DR. SHIVALEELA M.KUDARI)
© Rajiv Gandhi University of Health Sciences, Karnataka.
ACKNOWLEDGEMENT
I express my deep sense of gratitude to their great holiness Shri Jagadguru
Abhinava Shivananda Mahaswamiji for their divine blessings.
I express my sincere gratitude to the Principal Dr. G.B. Patil and management
committee for giving me the opportunity to pursue my post graduation studies in this
institution.
I express my deep sense of gratitude to my respected parents Smt. Sushila & Late
Shri Mallikarjun. S. Kudari, who filled the inner strength to me to achieve every mile
stone in my life.
I express my deep sense of gratitude to Dr. G.V. Mulgund MD (Ayu) (H.O.D), Dept
of Post graduate studies and Research in Dravyaguna, D.G.M.A.M.C Gadag. He has been
very kind to guide me in research and for whose extraordinary efforts and most valuable
advice made me to complete this work.
I would like to express my profound gratitude and extremely thankful to my guide
Dr. Kuber Sankh MD (Ayu) Professor Dept. of Post Graduate studies and Research in
Dravyaguna, D.G.M.A.M.C Gadag for his inspiring paramount thoughts, Zealous
suggestions, tremendous encouragement and most valuable guidance rendered for the
successful completion of this research work.
I express my sincere gratitude to Dr.Shashikant.B. Nidagundi M.D. (Ayu) Lecturer
Post graduate studies and Research in Dravyaguna, DGMAMC Gadag his most valuable
guidance and inspiration made me for the successful completion of this research work.
I Express my deep sense of gratitude to Dr. G.S. Hiremath M.D. (Ayu) PGARC
D.G.M.A.M.C. Gadag their most valuable guidance, inspiration & constant co-operation
at various stages of my research work.
I express my sincere thanks to Dr. Santosh Belavadi Lecturer, Dept. of
Panchakarma Post graduate studies D.G.M.A.M.C Gadag for their valuable guidance and
inspiration given at different stages of my work.
I am thankful to Shri. Shivakumar Inamadar Lecturer, K.L.E.’S College
Pharmacy Gadag, Shri Suresh Hiremath, Bhoomannavar Madam, Lecturer Dept of
i
Pharmacognosy & Shri Anant Bhandarkar Lecturer, K.L.E’s College of Pharmacy Hubli.
For their timely guidance & Help.
I express my sincere gratitude to Dr. U.V. Purad. H.O.D. Dept of Roganidana,
D.G.M.A.M.C. Gadag for their encouragement during the course of the study.
I am very much thankful to Deepa madam, Girish sir, Dept of Biotechnology for
their help in Phyto chemical analysis. I am very much thankful to Shri Nandakumar sir
for his help in statistical analysis of results.
I wish to convey thanks to my respected HOD’s of other Dept. Dr. M.C. Patil,
Dr. V.V. Vardacharyalu, Dr. Purushottamacharyalu, and Lecturers Dr.K.S.R. Prasad,
Dr. R.V. Shettar, Dr. Shivaramadu, Dr. Suresh Babu, Dr. K.S. Paraddi, Dr. Rajashekar,
Dr. Girish Danappagoudar, Dr. Shashidhar Doddamani, Dr. Jagadeesh Mitti, Dr.
Mulkipatil, Dr. Yasmin, Phaniband, Dr. Veena Kori, Dr. Samudri, & Dr. Shankargouda.
I am very much thankful to Dr. Annapurna & Dr Siddhalingesh. M. Kudari,
Lecturer B.V.V.S. Bagalakot for supporting me in preparing the dissertation right from
beginning to end.
I sincerely thank my beloved seniors Dr. K.S. Hiremath, Dr. Bani, Dr. Sajjanar,
Dr. Bingi, Dr. Sunitha. G. Dr. Jagadeesh Handiganur, Dr. Gangoor, Dr. C.B. Inamadar,
Dr. Doddamani, and special thanks to my classmates Dr. V.M. Katarki, Dr. Ashwini
Vastrad, Dr. Shalini Sharma, Dr. Rudrakshi, Dr. Suma, Dr. Jayashree, Dr. Kattimani, Dr.
Shivaleela Kalyani, Dr. Kamalakshi, Dr. Ashok, Dr. Sulochana, Dr. Madhushree, Dr.
Payapgoudar, Dr. Budi, Dr. Prasanna, Dr. Shiba,
I am thankful to junior friends Dr. Jaya, Dr. Savita, Dr. Kalavathi, Dr. Mukta,
Dr. Sevantika, Dr. Asha, Dr. Hiremath, Dr. Bhupesh, and other PG Department Seniors
and Juniors for their constant co-operation and help.
It is my privilege to express my gratitude & affection to my sisters Sarvamangala,
Savita, Jayashree & the respected Jijajis Shivabasav sobarad, Jayashubh Manvi, Suresh
Deshanur for their blessings to me in each and every step of my education & also who
filled the inner strength to me to achieve mile stone in my life.
I am highly indebted to my mother -in –law Smt. Lalita & Father-in-law
Fakkeerappa Hullur, for their co-operation and Help.
ii
I express great love towards my daughter spurti who has inspired me by her
cuteness and naughty activities.
I wish to convey my thanks to beloved librarian Shri. V.M. Mundinamani, Kerur,
Sureban and Shavi for providing me essential references in the study.
I am very much greatful to all lecturers house surgeons, Hospital staff and non
teaching staff for their timely assistance in completion of this work.
I am whole heartedly very greatful & dedicate this Dissertation work to my
respected Husband Mr. Siddhalingesh Hullur, and my daughter Spurti the prime
reasons for all my success.
Finally I thank God for making all those wonderful people happen to me & pray
for continued blessing and success.
Date:
Place: Dr. Shivaleela .M. Kudari
iii
ABBREVIATIONS
A. H. - Ashtanga Hridaya
A, K. - Amara kosha
A.P.I. - Ayurveda Pharmacopoea of India
Ab.R - Abhidhana Ratnamala
A. S - Ashtanga sangraha
B. N - Bhavaprakasha Nighantu
B. S - Bhela samhita
C. S - Charaka samhita
D. N - Dhanvantari Nighantu
D. G - Dravya Guna by P.V.Sharma
I.M.P - Indian Medicinal plants
K. N - Kaiyadeva Nighantu
K. S - Kashyapa samhita
Md.G - Madhava Dravyaguna
M. N - Madhava Nidana
Mh. N - Mahoushadha Nighantu
N. A - Nigantu Adarsha
R.N. - Raja Nighantu
S.S. - Sushruta Samita
Sha.S - Sharangaradhara Samhita
Sh. N. - Shaligrama Nighantu
V.S. - Vangasena
V.N. - Vanoushadhi Nidarshika
Y.R. - Yogaratnakar
iv
ABSTRACT
Background
Health and disease are the two faces of a coin. Ayurveda is the safest curative
system, The concept is to aid the human beings to provide healthy life and to prevent
diseases.
Inflammation can be correlated to shotha on the basis of equivalent symptoms
mentioned in the concerned literature. Inflammation is a symptom according to modern
system while Ayurveda signified it as a disease in accordance to shotha.
Inflammation is a common pathological condition, neither limited to age group
nor socio economical class of society.
Ayurvedic management measures seem to be more satisfactory, because of their
simplicity, applicability and easy availability and cost effectively.
Here the effect of Devadaru (Cedrus deodara) as shothahara (Anti-inflammatory)
has been carried out Devadaru has been mentioned as shothahara in all the Brahatrayees.
In this study Alcoholic extract and Aqueous extract of Devadaru has been taken
as test drug. They are compared with standard and control group with respective
parameters.
Objectives
1) Preliminary Phytochemical investigation of Devadaru[Cedrus deodara].
2) To evaluate the shothahara (anti-inflammatory] effect of Devadaru by
carrageenan induced Albino rats in four different groups.
3) To compare the shothahara effect of aqueous and Alcoholic extract of Devadaru
along with control and standard drug treated groups.
v
Method
In this experimental study randomly 24 rats are selected, made 4 groups & 6 rats
in each group, group I serves as control – Normal saline, Group II standard – Ibuprofen,
Group III – Aqueous extract of Devadaru, Group IV – Alcoholic extract of devadaru.
Inflammation is to be produced in to the sub plantar region of left hind paw of all
the rats with 0.1 ml carrageenan, the paw volume of each rat is measured with the help of
plethysmograph, after half, one, two and three hours.
Results
Both 3rd and 4th Group showed significant results but 4th group showed more
significant than 3rd.
Conclusion
In this experimental study the alcoholic extract of Devadaru has shown highly
significant anti inflammatory activity.
Key words
Shotha, Anti-inflammatory, Devadaru, Albino rats, Carrageenan, Plethysmograph.
vi
CONTENTS
Page No
1. Introduction 1-3
2. Objectives 4
3. Review of literature
A) Drug Review 5-17
B) Disease Review 18-60
4. Methodology 61-70
5. Results 71-96
6. Discussion 97-101
7. Conclusion 102-103
8. Summary 104-105
9. Bibliography 106-116
10. Annexure 117
11. Photographs
vii
LIST OF TABLES Table 1 DEVADARU
Page No.
Table 1.1 – Showing Gana and Varga according to different authors 05
Table 1.2 – Showing synonyms according to different authors 06
Table 1.3 – Showing Guna according to different authors 12
Table 1.4 – Showing Karma according to different authors 13
Table 1.5 – Showing Prayojy anga according to different authors 13
Table 1.6 – Showing Prayoga according different authors 14
Table 1.7 – Showing Matra according different authors 15
Table 2 DISEASE
Table 2.1- Showing Nidana of shotha according to different authors 21
Table 2.2 – Showing Purvarupa of shotha according to different authors 24
Table 2.3 – Showing Samanya lakshana of shotha according to different authors 25
Table 2.4 – Showing Lakshana of vataja shotha according to different authors 25
Table 2.5 – Showing Lakshana of pittaja shotha according to different authors 26
Table 2.6 – Showing Lakshana of kaphaja shotha according to different authors 26
Table 2.7 – Showing Lakshana of dvidoshoja shotha according to different
authors 27
Table 2.8 – Showing Lakshana of sannipataja shotha according to different
authors 27
Table 2.9 – Showing Lakshana of raktaja shotha according to different authors 28
viii
Table 2.10 – Showing Lakshana of Abhighataja shotha according to different
Authors 28
Table 2.11 – Showing Lakshana of vishaja shotha according to different authors 29
Table 2.12 – Difference between Acute and chronic inflammation 40
Table3 METHODOLOGY
Page No
Table 3.1- Showing Protocol of the experimental study 69
Table 3.2- Showing concentration and doses before induction of inflamation 69
Table 4 OBSERVATIONS AND RESULTS
Table No 4.1- showing the Phytochemical investigation of Devadaru 75
Table No: 4.2 showing Physico chemical values of Devadaru 76
Table No: 4.3 Results of Parameter 1st of all groups 81
Table No: 4.4 Summary of data of parameter 1st of all groupss 81
Table No: 4.5 ANOVA table for Parameter 1st between groups 81
Table No: 4.6 Comparison for Parameter 1st between the groups 81
Table No: 4.7 Results of Parameter 2nd of all groups 84
Table No: 4.8 Summary of data of parameter 2nd of all groups 84
Table No: 4.9 ANOVA table for Parameter 2nd between groups 84
Table No: 4.10 Comparison for Parameter 2nd between the groups 84
Table No: 4.11 Results of Parameter 3rd of all groups 87
Table No: 4.12 Summary of data of parameter 3rd of all groups 87
ix
Table No: 4.13 ANOVA table for Parameter 3rd between groups 87
Table No: 4.14 Comparison for Parameter 3rd between the groups 87
Table No: 4.15 Results of Parameter 4th of all groups 90
Table No: 4.16 Summary of data of parameter 4th of all groups 90
Table No: 4.17 ANOVA table for Parameter 4th between groups 90
Table No: 4.18 Comparison for Parameter 4th between the groups 90
Table No: 4.19 The mean of all the groups for all the parameters 93
LIST OF GRAPHS
Graph 1- Paw volume observed in individual rat of control group after 30 min 82
Graph 2- Paw volume observed in individual rat of standard group after 30 min 82
Graph 3- Paw volume observed in individual rat of trial group A (Aq extract)
after 30 min 83
Graph 4- Paw volume observed in individual rat of trial group B (Alc extract)
after 30 min 83
Graph 5- Paw volume observed in individual rat of control group after 1 hr 85
Graph 6- Paw volume observed in individual rat of standard group after 1 hr 85
Graph 7- Paw volume observed in individual rat of trial group A (Aq extract)
after 1 hr 86
Graph 8- Paw volume observed in individual rat of trial group B (Alc extract)
after 1 hr 86
Graph 9- Paw volume observed in individual rat of control group after 2 hrs 88
Graph 10- Paw volume observed in individual rat of standard group after 2 hrs 88
x
Graph 11- Paw volume observed in individual rat of trial group A (Aq extract)
after 2 hrs 89
Graph 12- Paw volume observed in individual rat of trial group B (Alc extract)
after 2 hrs 89
Graph 13- Paw volume observed in individual rat of control group after 3 hrs 91
Graph 14- Paw volume observed in individual rat of standard group after 3 hrs 91
Graph 15- Paw volume observed in individual rat of trial group A (Aq extract)
after 3 hrs 92
Graph 16- Paw volume observed in individual rat of trial group B (Alc extract)
after 3 hrs 92
Graph 17- Mean Paw volume of all group after ½ hr 93
Graph 18- Mean Paw volume of all group after 1 hr 94
Graph 19- Mean Paw volume of all group after 2 hrs 94
Graph 20- Mean Paw volume of all group after 3 hrs 95
MASTER CHART
1. Showing Assessment of Parameters I, II, III & IV of all groups 80
xi
LIST OF PHOTOGRAPHS
SL.No Name of the Photograph
1. Devadaru Tree
2. Stem bark of Devadaru
3. Aqueous extraction
4. Alcoholic extraction
5. Evaporation over hot plate
6. Aqueous extract & Alcoholic extract
7. Phyto chemical analysis
8. TLC Plate
9. Rats in cage
10. Oral administration of the drug.
11. Injecting carrageenan to left hind paw of rat.
12. Left hind paw Albino rat after inducing inflammation.
13. Measurement of inflammation using plethysmograph.
xii
Introduction
INTRODUCTION
Ayurveda is a science of life with two main objectives maintenance and
promotion of positive health and cure of the diseases. Ayurveda is believed to be
prevalent since 5000 years in India. In 1974 w.h.o. recognized Ayurveda the Indian
traditional medicine and requested to improve the service and availability of
ayurvedic drugs in our country. This traditional medicine is much popular for curing
the most of the diseases.
Among the countless number of ailments in this world a few can be identified
as very common and recurrently affecting, where inflammation is also one of those.
Inflammation is mentioned in modern system of medicine as a symptom rather than a
disease. Ayurvedic references have showed it is a disease entity by explaining the
following Samprapti in other word the Pathogenesis.
“Vatadosha undergoing increase, pushes out the increased Rakta, pitta, and
kapha to exterior (twak) by blocking their channels and produces swelling of skin and
muscles (twak, mamsa). It is called Utseda, Samhata, Shotha in view of increased
size.” (Ma.Ni.36th chapter). It is an important entity and has a nearer meaning to the
kind of inflammation.
It is believed that every dravya available on this earth has medicinal property
in it; only thing should be used rationally. Further more it is said that even a poison
can be good medicament if used with caution.
In Ayurvedic texts inflammation has been described under various terms like
Shotha, Shopha, Shwayatu, Vrana shotha. But the term shotha is used specially for
inflammatory swelling.
It is self protective reaction of the tissue towards infection, irritants or foreign
substances. Though it is a part of host defense mechanism when it becomes great it
Anti Inflammatory effect of Devadaru 1
Introduction
turns to be a hopeless condition, which cause tissue damage. Similarly the
exaggerated inflammatory reaction also do harm to the body. Therefore the timing of
inflammation is essential.
It is also oftenly associated with changes that affect the body as a whole in
particular with leucocytosis and pyrexia. Inflammatory process involves a series of
events that can be elicited by numerous stimuli (infection, antigen antibody reaction,
physical or thermal injuries) efforts to control shotha or inflammation where the time
of Sushruta. Its importance and vastness can be well understood by the voluminous
work done by him on this subject. He has dealt with this entity efficiently from
different angles and described a range of ganas in detail to treat shotha. Not only
Sushruta even Charaka has also mentioned Shothahara dravyas and its ganas along
with various measures to deal with it.
Anti-inflammatory drugs of modern medicine are affective but have number of
side effects causing gastric erosion, haemorrhage etc. Inflammatory drugs are
classified
Non-Steroidal Anti-Inflammatory Drugs (NSAID)
Steroidal Types.
The chemicals which are comes under this headings can produce undesired
effect in therapeutic usage includes interstitial nephritis, hepatic cell damage, fluid
retention, skin rashes etc. By continuous usage of steroids will disturb the
physiological system and causes the multiple complications. To combat these
problems it is necessary to evaluate plant based anti-inflammatory agents.
There are many inflammatory drugs described in AYURVEDIC Literature,
among them Devadaru [Cedrus deodara] is one of the most potent anti inflammatory
drug, .
Anti Inflammatory effect of Devadaru 2
Introduction
Devadaru [Cedrus deodara] is the big tree of family pinaceae mainly found in north
western Himalayas, having the properties like, tikta rasa laghu snigda guna, ushna
veerya, katu vipaka, acts as kaphavata shamaka and indicated in vibandha, admana,
shotha, ama tandra, hikka, jwara, rakta dosha, prameha,peenasa, kaphaja kasa and
kandu.
The parts used in this drug are kashta and taila. The major chemical constituents of
essential from wood are P-methyl aceto phenone, sesquiterpenes, stembark cotains
deodarin,toxifolin. Its local application and oil are used in arthritis, its oil is very good
wound cleaner and healer.
In present study an attempt is made to preliminary phytochemical investigation of
cedrus deodara extraction were conducted and observed the presence or absence of
alkaloids, proteins, carbohydrates, steroids, saponins, tannins, resin, starch, oils, and
fats and TLC methods were done. During experimental study total 24 albino rats were
taken and subjected them in four groups [Group I to IV]. Group I was control group.
Group II was standard group, Group III was Trial Group A with Aqueous extract and
group IV was Trial group B with Alcoholic extract, After induction of carrageenan
immediately inflammation was observed and measerd then compared the
sthothahara[anti inflammatory] effect of aqueous extract and alcoholic extract of
Devadaru along with control and standard drug treated groups.
Anti Inflammatory effect of Devadaru 3
Objectives
OBJECTIVES OF THE STUDY :
1. Preliminary Phytochemical investigation of Devadaru (Cedrus deodara)
Extraction
Chemical analysis - Test for alkaloids, flavonoids, triterpenoids,
glycosides, steroids, saponins, tannin, carbohydrate, proteins, resin,
starch, oils and fats.
Thin layer chromatography (TLC)
2. To evaluate the shothahara (anti inflammatory) effect of Devadaru by
carrageenan induced paw oedema method14 .
3. To compare the shothahara (anti inflammatory) effect of aqueous extract
and alcoholic extract of Devadaru along with control and standard drug
treated groups.
Anti Inflammatory effect of Devadaru 4
Drug review
DRUG REVIEW
Historical aspect of the Drug (Drug)1
In Parasara grhya sutras and kousika sutras we come across the references
about Devadaru (P.G.S. 1/19 & Kou, su 58/16). Panini also quoted regarding
Devadaru vanam (P.M. 8/4/18).
Table No. 1.1 Ganas and vargas according to different classics.
Charaka samhita Stanya shodhana
Anuva sanopaga
Katukaskandha
Sushruta samhita Vata samshamana
Eladi gana
Rakta sravaka varga
Astanga hriday Niruhana varga
Vata samshamana varga
Vachadi varga
Eladi varga
Bhavaprakasha Nighantu Karporadi varga
Nighantu Adarsha Devadarvadi varga
Kaiyadev Nighantu Aushadhi varga
Raj Nighantu Chandanadi varga
Dhanvanatari Nighantu Guduchyadi varga
Madanapala Nighantu Abhayadi varga
Shaligram Nighantu Kapooradi varga
Abhidana Ratnamal Tikta dravya skanda
Madhava dravya guna Vividoushadhi varga
Amara kosha Vanoushadi varga
Anti Inflammatory effect of Devadaru 5
Drug review
Table No. 1.2 Paryayas according to different authors
Synonyms C2 S
S3 S
A4 H
B5 N
K6 N
R7 N
D8 N
M9 N
N10 A
Ab11 R
A12
K S13
N M14
N Indradaru - - - + - - - - - - + - - Masta daru - - - + - - - - - - - - - Drukilima - - - + - - - - - - - - - Kilima - - - + + - + - + - - + + Darubhadra - - - + - - - - + - - + - Surabhuruha - - - + - - - - - + - - - Surahva - - - - + - + + - - - - - Snehaviddha - - - - - - + - - - - - - Mahadaru - - - - - - + - - - - - - Bhadradaru - - - - + + + + + - - + + Devakashta - - - - + - + - - - - - - Puthikashta - - - - - - + - + - - + - Sudaru - - - - - - + - - - - - - Suradaru - - - - - - + - - - - + - Indravruksha - - - - - - + - - - - + - Amaradaru - - - - - + + - - - - + - Suradruma - - - - + - - + - - - + - Bhadrakashta - - - - + - - + - - - - - Snehavruksha - - - - - - - + - - - + - Krimila - - - - - - - + - - - - - Shakradaru - - - - - - - + - - - - - Daruka - - - + - - - - - - - - - Snigdadaru - - - - - + - - - - - + - Shivadaru - - - - - + - - - - - + - Shambhava - - - - - + - - - - - + - Bhutahari - - - - - + - - - - - + - Bhavadaru - - - - - + - - - - - + - Rudradaru - - - - - + - - - - - - - Shakadru - - - - + - - - + - + + - Peetadru - - - - - - - - + - - - - Shakrapadapa - - - - - - - - + - - + - Paribhadraka - - - - - - - - + - - + - Peetadaru - - - - - - - - - - - + - Surahvaya - - - - - - - - - - - + - Bhadravat - - - - - - - - - - - + - Shatapadapa - - - - - - - - - - - + - Kalpapadapa - - - - - - - - - - - + - Daruka - - - - - - - - - - - + - Surakashta - - - - - - - - - - - + - Devadaru + + + + + + + + + + + + + Daru + + + + + - + - + - +
Anti Inflammatory effect of Devadaru 6
Drug review
Paryayas and its meanings15
1. SåuÉSÉÂ : Himalaya isGod’s country where this tree is grown
(V.M.G)
2. pÉSìSÉÂ : Good Fragrant wood (V.M.G)
3. xÉÑUpÉÔÂWû : The tree which grows in God’s country (P.V.S)
4. mÉÏiÉSìÓ : mÉÏiɶÉÉ SìÓÓ¶ÉåÌiÉ | mÉÏrÉiÉå cɤÉÑwÉÉÅrÉqÉç CìÌiÉ | (N.A)
Its kashta is yellow in colour. Its beauty is perceived
through the eyes.
5. mÉÔÌiÉMüɸ : mÉÔiÉå: mÉÉuÉlÉxrÉ MüɸqÉç CìÌiÉ | (N.A)
Its kashta iradicates bad smell.
6. mÉÉËUpÉSìMü : mÉËUÌlɹÉmÉëÉmiÉÇ pÉSìqÉ AxrÉ mÉÉËUqÉSì: |
mÉÉËU ÌlÉ¹Ç mÉëÉmiÉ pÉSìèqÉxrÉåÌiÉ | (N.A)
Its sevana causes paripurna kalyana
7. zÉ¢ümÉÉSmÉ : zÉ¢üxrÉ CuSìxrÉ mÉÉSmÉ: uÉפÉ: CìÌiÉ |
This is the tree of Indra
8. pÉSìSÉ : pÉSìÇ SÉ CìÌiÉ | (N.A)
Its kashta is best among all the kashtas.
9. ÌMüÍsÉqÉ : ÌMüsÉÌiÉ ¢üÏQûÌiÉ sÉbÉÑiuÉÉiÉç | (N.A)
Beacause of its light weight moves freely.
10. mÉÏiÉSÉ : mÉÏiÉÇ cÉ iÉSèSÉ cÉ CÌiÉ, mÉÏiÉÇ SÉÂxrÉåÌiÉ uÉÉ |
Its Kashta is having peetavarna (N.A)
11. SåuÉSÉ : SåuÉÉlÉÉÇ SÉ CìÌiÉ; SÉÂhÉÉÇ uÉÉ SåuÉ: CìÌiÉ; (N.A)
Its kashta resembles God so it is shreshta.
Anti Inflammatory effect of Devadaru 7
Drug review
12. SÉ : SÉUrÉÌiÉ ÌuÉoÉlkÉÉÌS UÉåaÉÉlÉç CìÌiÉ | (N.A)
It iradicates vibandhadi rogas.
13. mÉÔÌiÉMüɹ : mÉÔÌiÉ EaÉëaÉÇlkÉ MüɹqÉç AxrÉ CìÌiÉ | (N.A)
Its kashta is having Ugragandha.
Vividha Bhasha naam (Vernacular Names)
Latin Name : Cedrus deodara
Sanskrit : Devadaru, Badradaru, Suradaru, Snehavidda, Vrika
shapa.
Hindi : Devadar, Deodar, Toona
Marathi : Devadar
Gujarathi : Devadar
Telagu : Devadari
Kannada : Devadar
Bengali : Devadaru, Toon
English : Deodar, Pinus Deodara, Himalayan cedar.
Tamil : Toon – maram, Devadaru
Malayalam : Devadaru
Punjabi : Pahari – keli
Arabic : Sanobarulhind, Shajratudde vadar
French : Deodar
Afghanistan : Imanza, Nikhtar
Garhwal : Dadar, Deodar, dewadar, Diar
Kashmir : Dadar, Dar, deodar.
Urdu : Deodara
Himalaya : Kalu, Keoli, Kilar Kilei.
Anti Inflammatory effect of Devadaru 8
Drug review
Botanical Classification
Kingdom Plantae
Sub Kingdom Tracheobionta
Division Coniferophyta
Class Pinopsida
Order Pinales
Family Coniferae
Genus Cedrus
Species Deodara
Family 16
Kula : Devadaru kula
Family : Coniferae
CONIFERAE
Trees or shrubs, usually resinous, mostly evergreen. Leaves usually needle-
like or scale-like, rarely with a broad blade; stipules 0. Flowers monoecious or
dioecious, perianth 0. Male flowers in deciduous catkins consisting of stamens which
are usually scale- like and bear 2-6, rarely more, 1-celled pollen-sacs on the lower
surface. Female flowers in cones, consisting of scale-like open carpels which are flat
or peltate and bear either directly or on a special subsidiary scale (placental scale) 1-2
many ovules or the female cone reduced to a single ovuliferous scale or to a single
ovule. Fruit usually a woody cone sometimes berry-like or formed from the ovule
alone in which case the outer coat usually becomes fleshy. Embryo with 2-16
cotyledons.- Throughout the world, chiefly in cold regions.
A. Scales of the female cone opposite, in several series. Leaves Very short of subulate
1. Scales of cone woody; testa winged …………………. Cupressus.
Anti Inflammatory effect of Devadaru 9
Drug review
2. Scales of cone cohering into a globose berry-like fruit enclosing the seeds;
testa hard not winged…………. Juniperus.
B. Scales of female cone or spike few. Leaves scattered or bifarious
1. Leaves persistent, in bundles of 2,3 or 5, narrowly linear.
Scales of cone persistent……………………………. Pinus.
2. Leaves persistent, in bundles of many, acicular, scales of erect cone deciduous
…….. Cedrus.
3. Leaves more or less distichous, linear. Scales of large erect cone deciduous
.The bark and leaves are astringent; the resin and the essential oil are
stimulant, diuretic, and anthelmintic.
The glucoside coniferin occurs in the cambium sap of coniferous trees; thujin
occurs in Thuya.
A toxic alkaloid, taxine, has been isolated from the leaves, shoots, and fruits of
the yew. Other toxic substances obtained from members of this order are formic
acid, oil of savin, oil of yew.
Swaroop (Botanical Descriptions)17
A large evergreen tree of height 85 mtrs.
Kanda (Stem) : Big erect having circumference 12 mtrs.
Twak (Bark) : Thick and cracked.
Patra (leaves) : are green, elongated with tapering ends.
Pushpa (Flowers) : Green, Yellow and appear in clusters.
Phala (Fruit) : Ripe fruit is black having seed 1 cm. Long
The tree bears new fruits in October, which ripe within a year.
Deodar true has a long life having life span of 600 years.
Anti Inflammatory effect of Devadaru 10
Drug review
Botanical description according to modern18
Cedrus deodara is a large evergreen tree. It grows up to the height of 250 feet.
Branches – Not whorled the leading shoot and tips of the branches usually drooping.
Bark – Dark sometimes almost black usually very rough on oil stems, some time only
lightly furrowed.
Stem – Straight and wide usually of 36 feet circumference, The branches at the above
are small sequence, From far away it looks like a triangle shape.
Shoots – Dimorphic, long shoots with the needles solitary and arranged spirally.
Leaves – 2.5 – 3.8 cm long, needle like, triquetrous, sharp pointed.
Flowers – Usually monoecious, but some tree or branches habitually bears flower of
one sex, male catkins solitary at the end of the branches, Female flowers in cones,
which are solitary at the end of branches.
Fruits – are 4-5 inches long and 3-4 inches breadth & raised. The apex is rounded and
has many scales, its edges are thin.
Seeds – are 7.5 15mm long, pale brown wing longer, then the seeds are triangular in
shape and sides are rounded.
The fruits occur in October month and ripe in 1 year. The age of devadaru is generally
600 years.
Habitat19
Devadaru grows mainly in North-westernHimalayas from Kashmir to Garhwal.
Forests of Deodar found in Kashmir, kulu, chamba, Tehri – Garhwal,simla, Almora
and Mussoorie hill stations.
Bedha according to different authors:
According to Raj Nighantu & Shaligram Nighantu20,21
Snigdadaru, Kashta daru
Anti Inflammatory effect of Devadaru 11
Drug review
Snigda daru – It has thick and oily wood & available in the market in the name of
‘Dhoopa’
Kashta daru – Ashoka tree is known as kashtadaru the leaves of this tree are used for
festive occasional its latin name is Polyalthia longifdia, Anonaceal family i.e
sitaphalakula.
Table 1.3 Gunas (Properties) According to different author.
Properties B22
N
D23
N
M24
N
R25
N
K26
N
N27
A
S28
N
Vanoushadhi29
Nidarshika
P.V. Sharma30
Rasa
Tikta + + + + + + + + +
Katu - - + - + - - - -
Guna
Laghu + - - - + - + + +
Snigda + + + + + + + + +
Veerya
Ushna + + + + + + + + +
Vipak
Katu + - + - + + + + +
Doshaghnata
Vatahara + + + + + + + + +
Kaphahara + + + + + + + + +
Chemical Composition
Wood oil contains oleo-resin, essential oil, and needles (leaves) contain
ascorbic acid. Essential oil from wood: Premethylacetophenone, atlantone,
sesquiterpenes (α&β himochalene, himachalol etc); stem bark: deodarin, toxifdin 31.
Anti Inflammatory effect of Devadaru 12
Drug review
Table 1.4 Karmas according to different authors.
Karmas C32
S
S33
S
A34
H
BP35
N
D36
N
R37
N
K38
N
N39
A
RS40
A
M41
N
P.V.S42 Van
Dar43
Shothahara + + + + + + + + + + + +
Karnashoolahara - + - - - + - - - - + +
Hikkanigrahana + - - - + - - - - - + +
Varnashodhana - + - - - - - - - - + +
Vrana ropana - + - - - - - - - - + +
Rakta prasadana - - + - - - - - - - + -
Deepana - - - - - - - - - + + +
Pachana - - - - - - - - - + + +
Krimighna - - + - - - - - - - + -
Anulomana + + + + - + - - + - + -
Swedajanana - - - + - - - + - - - -
Vedanastapana + + + + - + - - - - + +
Kandughna - - - + - - + - - - + +
Mutrajanana - - - - - - - - - - + +
Stanyashodana - - - + - + - + + - + +
Jwaraghna - - - - - - - - - - + +
Lekhana - - - - - - - - - - + +
Rasayana - - - + - - - - - - - -
Amapachaka - - - + + + - - - - + +
Hridayattejaka - - - - - - - - - - + +
Kushtaghna - - - - - - - - - - + +
Pramehaghna - - - + - - - - - - + +
Table 1.5 Prayojya anga
Part used DG44 P.V.S
R45 N
B46
N N47
A Pharmacopoea48
indica DG49 V.M.G
Van Dar50
Kashtasara + + + + - + + Taila + + + + + + + Bark - - - - + - -
Anti Inflammatory effect of Devadaru 13
Drug review
Table No. 1.6 Prayoga according to different authors.
Prayoga C51
S
S52
S
A53
H
BP54
N
K55
N
R56
N
M57
N
D58
N
N59
A
S60
N
D.G
P.V.S61
D.G62
J.L.N
Vibandha - - - + + + - + - - + -
Admana - - - + + + + + - - + +
Shotha + + + + + - + - + + + +
Tandra - - - + - - - - - - - -
Hikka + - - + + - + - + - + +
Jwara - + - + + + + - + + + +
Prameha - - - + + + - +` - - + +
Peenasa - - - + + - - - + - - +
Kasa - - + + + - - - + - + +
Kandu - - - + + - + - - - + +
Amavata - - - + + - + - - - + +
Shirahashula - - - + - - - - - - - -
Shleepada - - - + - - - - - - + -
Jalodara - - - + - - - - - - - -
Shwasa + - - + + - - - + + + +
Atisara - - - + - - - - - - + -
Ashmari - - - + - - - - - - + -
Vrana - - - + - - - - - - + -
Kushta - - - + - - - - - + + +
Karnashoola - - - + - - - - - - - -
Raktavikara - - - + + - - - - - + -
Aaamavikara - - - - - + - + - + + -
Arsha - - - - - + - - - - + -
Bhootabadha - - - - - + - - - - - -
Vruna - - - - - - - - - + - +
Shleepada - - - - - - - - + - - -
Kushta - - - + + - - - + + + -
Karnashoola - + - - - - - - + - + -
Krimi - - + - - - - - + - + -
Anti Inflammatory effect of Devadaru 14
Drug review
Action and uses in other system of medicine63
Unani – Hot 2, Dry 2, Resolves inflammation, antispasmodic, anti-poison, paralysis,
stone in the kidney, fevers.
Oil: Hot - 20, Dry – 10, for injuries (external).
Action:
Wood is carminative, bark is powerfully astringent and febrifuge. Leaves have
mild terebinthinate properties.
Uses:
Bark is a good remedy in remittent and intermittent fevers, diarrhoea and
dysentery and though not bitter it is a fair substitute for perurian bark particularly
when united with powdered Bonduc nut. Its powder is applied with much benefit in
the treatment of ulcers. It is considered especially useful in bilious fevers and
inveterate diarrhoea arising from atony of the muscular fibre.
Oleo-resin and dark coloured oil or turpentine, are applied to ulcers and skin
diseases. They are valuable in manage in horses and sore feet of cattle.
Controverisial studies64
Thakuriji is of the opinion that pinus species such as P excelas wall and even
P. Longifolia Roxb are known as kaila and kolaina respectively at Garhwal, It is
therefore, possible that kilima supposed to be synoym of Devadaru by charaka may be
a varity of sarala.
Table 1.7 Matra (Posology)
D.G65
P.V.S
D.G66
Hastamalaka
D.G 67
(V.M. Gogle)
Powder 3-6 gm 1-3 gm 1-3 Gm
Oil 20-40 drops 10-20 drops 20-40 drops
Anti Inflammatory effect of Devadaru 15
Drug review
Therapeutic uses 68
Charaka – Hikka & Shwasa – The decoction of Devadaru should be given
(Ch.Chi, 21-112)
Sushrut -= Jwara – Decoction of devadaru is given
Shotha – Decoction of devadaru is given with Gomutra is givens.
Vagbhata – Kaphajakasa – The cloth which is dipped in the oil should be roll over
the cedar wood and burnt while burning the oil drops
comes from it, To this oil, yavakshara & Trikatu are
mixed The preparation destroys kaphaja kasa.
Hareeta – Vatajanya vruna – Devadaru & Shunti are rubbed & the paste is applied
over the wound.
Chakradatta – Shleepada – Chitraka moola & Devadaru oil are powdered & mixed
with Gomutra, then by applying the paste it gets relief.
Vangasena – Kaphajanya Gandamala – Devadaru and Indravaruni moola are
pasted with water & applied.
Shleepada – Devadaru choorna with sarshapa taila is given.
Shodhala – Kushta – By burning Devadaru moola one type of Rasa will get if it is
taken with dugda all types kushta will iradicate.
Karnashoola – The cloth which is dipped in the oil is roled over the cedar wood &
burnt by burning one type of Rasa or Taila is extracted. This taila
relieves karna shoola.
Pilla namaka Netra roga – To Devadaru sukshma choorna Ajamutra bhavana is
given then it is used as Anjana for netra roga.
Rasahrudaya tantra – Peenasa – Devadaru taila with Goghrita is given.
Anti Inflammatory effect of Devadaru 16
Drug review
Formalutions of Devadaru
• Devadarvyadi kwatha
• Devadarvadi choorna
• Devadarvadyarishta
• Rasanadi kwatha
• Satyadi choorna
• Karanjadi yoga
• Rasana panchak kwatha
• Punarnavadi mandoora
• Vishagarbha taila
• Chandra prabha vati
Research Works69
• The alcoholic extract of the stem was found to have anticancer activity against
human epidermal carcinoma of the nasopharynx in tissue culture ( 1968).
• Stem bark etxtract showed significant anti-inflammatory activity in
rat.(Ind.J.Pharmacol 1973).
Anti Inflammatory effect of Devadaru 17
Disease Review
DESEASE REVIEW
SHOTHA (SHOPHA)
NIRUKTI
The word shotha is derived from the root “Savagathou Bahulakath Pha” which
means instantly spreading.
“Shwayathu” is derived from the root word “Do aswigativridyah” which means by shich
the body is bulging70.
When AjÉÑcÉ mÉëirÉrÉ is added to the aÉÌiÉuÉ×̬AjÉïrÉÑ£ü OÒûAÉåꦃ kÉÉiÉÑ The word shotha is derived71.
“Shotha” “Shwayathu” “Shopha” very marked swelling of the skin on any place is to be
under stood.
PARIBHASHA
Shotha is a disease caused due to the Derangement of Doshas, which may appear
at any part of the body involving Twak and mamsa. It is characterized byswelling, pain,
Redness and raised local temperature.
‘Shotha’ is found as a main symptom in many number of ailments like Granthi,
vidradhi, Alaji etc. But that which is going to spread vastly, which is nodulated, equal or
unequal (Sama or Vishama) and particularly located dosha-samuha in the Twak (skin)
and Mamsadi dhatus (tissue elements) is Shotha72.
NIDANA
Causative factors for endogenous type of Inflammation are as listed below
according to different classical references;
According to Charaka
1. Consumption of kshara (alkaline preparation) amla (Sour food and drinks),
tikshna (articles of food and drinks having sharp attribute), ushna (hot food and
Anti Inflammatory effect of Devadaru 18
Disease Review
drinks) and guru (heavy food) by a person who is weak and emaciated because of
shodhana (Elimination therapy of Panchakarma).
2. Intake of curd, uncooked food, mrut (mud) shaka (leafy vegetables), virodhi anna
(Ingredient of food having mutually contradictory properties), dushta anna
(polluted food including water in the beginning of rainy season) or food afflicted
with gara (artificially prepared poison).
3. Afflictions with arsha (piles) and lack of exercise.
4. Administration of elimination therapies in improper time.
5. Irregular delivery including abortion and miscarriage.
6. Inappropriate administration of elimination therapy and improper care of the
patient after the administration of these therapies.
Another opinion of Charaka is- Hardship of the external skin by the Abighatha of
wood, stone, weapon, fire, poison and iron equipments gives leads to prakupita of doshas,
these doshas vitiates twacha gives rise to rise to exogenous type of inflammation.
Similar opinion is expressed by Sushrutha and Vagbhata. Along with all the above
factors Vagbhata adds that - doshas localised in the chest produces inflammation in the
upper part of the body, those prevailing in the region of the urinary bladder, produce
Inflammation in the lower parts of the body, those localized in the middle part produce
inflammation in the middle part of the body; those which are spread all over the body will
produce inflammation of the whole body and localized in any one part will cause
inflammation of that part only.
Nija Shotha Nidana:
Samanya Laxanas include etiogenic factors like- Improper performance of
Pancha Karma; Mithya Samsarjana Krama; Secondary conditions like Chardi (caused by
Anti Inflammatory effect of Devadaru 19
Disease Review
Vega Dharana) and Roga janita Karsya. Improper Habits like Upavasa, Vega Dharana,
Ati Guru-Amla- Lavanadhi ahara sevan. Gyneic Factors- Garbhapata (miscarriage), Ama
garbhapatana (abortion); Prajatanam Mithya-apacharat (improper hygiene during
puerperal period).
Vishishtha nidana of Vataja shotha: Ahara- Seeta-Ruksha-Laghu-Vishada
Padarthadi sevanam. Vihara- Shrama, Upavasa, Kshanana.
Vishishtha nidana of Pittaja shotha: Ahara-Ushna-Teekshna-Katu-Kshara-
Lavana-Ajirna Bhojana. Vihara-Agni-Atapa prapata.
Vishishtha nidana of Kaphaja shotha: Ahara- Guru-Madhura-Sheeta-Snigdha
bhojana. Vihara-Ati nidra, Avyayama etc.
Agantuja Shotha Nidanam:
(Injuries: Chedana (excision), Bhedana (cutting), Bhanjana (scalding), Prahar
(beating), Bandhana( tourniquet), Pedana (pressing), Vyadhana (incision) etc., caused by
the sastras (instruments etc.).
Vegetable Sources: Bhallataka, Kapikacchu, Poisonous leaves, Poisonous
climbers /shrubs etc.
Animal Sources : Krimi Suka, Swedana, pari sarpana, Visha pata of poisonous
animals, bite or sting of poisonous animals or the injury caused by the teeth or horns.
Environmental Sources : Sagara vata, Visha Vata, Hima sparsha, Agni sparsa etc.,
factors well known to cause inflammation.
Anti Inflammatory effect of Devadaru 20
Disease Review
Table No. 2.1 ÌlÉSÉlÉ
cÉUMü73 xÉÑ´ÉÑiÉ74 uÉÉapÉOû75 1) Improper performance panchakarma 2) Kshara, Amla, Lavana, Tikshna, Ushna, Guru padarta sevana. 3) Apakvanna, Viruddanna, Dooshitaanna, Kritrimavishayukta anna sevana. 4) Affliction by Arsha 5) Vishama prasuti, Garbhapatana, Mudhagarbha 6) Afflication of external skin by the impact of kaasta, ashma, shastra, agni, visha and ayasa implements.
1) Walking after taking the food 2) Guruanna, Shaka, Lavanapradana bhojana, 3) Durbala vyakthi in adhika matra amla padarta sevana, anupa mamsa, ajeerna. 4) Adhika sthree prasanga. 5) Viruddha ahara sevana 6) Riding on horse, camel, chariot,
1) The person who has become week by diseases, therapies, fasting etc, 2) Indulging suddenly in large amount of food or those foods which are guru, amla, snigdha, sheeta, lavana, shara, tiekshna, ushna, shaka, ambu, nidra, ratri jagarana, eating mud, fatigue copulation. 3) Walking long distances holding flags & banners 4) Riding on vehicle and such other strenous acts. 5) Suffering by diseases such as Kasa, Shwasa, Atisara, Chardi, Jwara, Visuchika, Alasaka, Pandu, Visarpa etc.
SAMPRAPTI
According to Charaka:
Charaka has mentioned separate Samprapti for Agantuja and Nija shotha.
Agantuja shotha Samprapti:
The Aganutuja shothas are diagnosed by the characteristic etiology, signs and
symptoms even though ultimately the Agantuja shotha may share the characteristic signs
and symptoms of Nija shotha. The difference lies in the priority or post priority of certain
features common to both type of shotha. The Nija shotha starts with the vitiation of
doshas and then brings about pain. The Agantuja shotha on the other hand starts with pain
and then brings about the vitiation of dosha.
Anti Inflammatory effect of Devadaru 21
Disease Review
Nija shotha samprapti
Because of the Nidan-Kapha, Rakta, Pitta enters in the external vessels and
afflicts Vayu localized there, as a result of these factors the passage (channels of
Circulation) get obstructed which spread to nearby areas, thereby causing inflammation.
If these affliction takes place in the chest region, then the inflammation occur in
the upper part of the body (urdhva shotha). If these afflictions takes place in the colon or
pelvic region which is the location of vayu, then the inflammation occurs in the lower
part of the body ( adhah shotha); if these afflictions takes place in the middle part of the
body that is between chest and pelvic region then occurs in the middle part of the body
(Madhya shotha) and if these afflictions takes place all over the body then the
inflammation occurs all over the body (sarvanga shotha) if however these afflictions are
located in any particular viscera, such as throat and palet then inflammation takes place in
that locality and it is designated after the name of the viscera where it occurs (e.g, gala
shotha)76.
According to Vagbhata:
Vata getting increased brings the vitiated pitta, rakta and kapha into the external
channels and getting obstructed by them, produces inflammation localized in the skin and
muscle called utsedha, samhata and shotha77
According to Madhavakara:
Vata undergoing increase pushes out the increased rakta, pitta and kapha to the
exterior (twak skin) by blocking their channels and produces shotha (swelling) of the skin
and muscle (twak mamsa) it is called as Utseda, Samhata and Shotha in view of its
increased size78.
Anti Inflammatory effect of Devadaru 22
Disease Review
Schematic representation of Shotha samprapti
Nidana
Vatadosha gets vitiated
Vatadosha vitiates rakta pitta & kapha doshas
Vayumargavarodha
Utsedha
Shotha
BHEDA
According to Charaka79
Even though all the three doshas involved in the manifestation of all the types of
the Shotha, it is on the basis of the predominance of the respective doshas that vataja,
pittaja and kaphaja varieties of disease are determined and therapies are prescribed
accordingly.
All the varieties of the inflammation are considered to be tridoshaja i.e. they are
caused by the vitiation of all the three doshas even so the causes of inflammation differs
from one to another according as the particular dosha which is predominantly vitiated.
The physician should therefore determine the line of treatment according to the
predominance of one dosha or the other.
1) On the basis of Dosha
a) Vataja b) Pittaja c) Kaphaja
2) On the basis of Karana
a) Nija b) Agantuja
3) On the basis of Sthana
a) Ekangaja b) Sarvangaja
Anti Inflammatory effect of Devadaru 23
Disease Review
c) - Inflammation pervading the whole body.
- Inflammation pervading the half of the body.
- Inflammation afflicting only one limb of the body.
According to Susrutha80:
As the Shotha develops from the six factors as vata, pitta, kapha, rakta,
sannipatika, agantuja that are the types so called to be the six as Vataja, Pittaja, kaphaja,
Raktaja, Sannipataja and Agantuja .
Depending upon signs, symptoms and treatment earlier six types has been
explained but sarvasara that is the shotha which spread all over the body are of 5 type that
is Vataja, Pittaja, kaphaja, Sannipataja and Vishaja.
According to Vagbhata & Madhavakara81-82:
Based on different causes and symptoms it is of nine types from each dosha
separately, from the combination of two doshas and from the combination of all them,
from trauma/injury and from the poison.
Mainly, it is of two types;
a) Nija, Agantuja
b) Sarvanga, Ekanga
It is known to be of three types
a) Prthu (hard)
b) Unnata (raised/elevated) c) Grathita (glandular) .
PURVA RUPA Table No. 2.2 mÉÔuÉï ÂmÉ
cÉUMü83 xÉÑ´ÉÑiÉ uÉÉapÉOû84
FwqÉÉ SuÉjÉÑ ÍxÉUÉhÉÉqÉÉrÉÉqÉç
---
SuÉjÉÑÈ ÍxÉUÉhÉÉqÉÉrÉÉqÉç AÇaÉ aÉÉæUuÉ
Anti Inflammatory effect of Devadaru 24
Disease Review
SAMANYA LAKSHANA
Table No. 2.3 xÉÉqÉÉlrÉsɤÉhÉ
cÉUMü85 xÉÑ´ÉÑiÉ uÉÉapÉOû aÉÉæUuÉ AlÉuÉÎxjÉiÉ EixÉåkÉ FwqÉÉ
ÍxÉUÉiÉlÉÑiuÉÇ sÉÉåqÉWûwÉï ÌuÉuÉhÉïiÉÉ
---
---
VISHESHA LAKSHANA
Table No. 2.4 Vataja shotha:
ÌuÉÍvɹ sɤÉhÉ cÉUMü86 xÉÑ´ÉÑiÉ87 uÉÉapÉOû88 uÉÉiÉeÉ vÉÉåjÉÈ cÉsÉ
iÉlÉÑ iuÉMçü mÉÂwÉ xÉÑÎmiÉ
WûwÉï vÉÉåjÉ (Divabali)
AÂhÉ M×üwhÉ mÉÂwÉ qÉ×SÒ iÉÉåS
cÉsÉ Ã¤É AÂhÉ, M×üwhÉ uÉhÉï MüMïüzÉUÉåqÉrÉÑ£ü xÉlMüÉååcÉ xmÉlSlÉ iÉÉåS Swelling increases and decreases quickly soon spreads to other part of the body Subside by massaging with fatty and hot oil mild at night and severe during day time
Anti Inflammatory effect of Devadaru 25
Disease Review
Table No. 2.5 Pittaja Shotha:
cÉUMü89 xÉÑ´ÉÑiÉ90 uÉÉapÉOû91 ÌmɨÉeÉvÉÉåjÉ qÉ×SÒ
xÉaÉlkÉ M×üwhÉ or mÉÏiÉ uÉhÉï pÉëqÉ, euÉU, xuÉåS, iÉ×whÉ, qÉS Tenderness in affected part Eyes becomes red Excessive burning-sensation.
mÉÏiÉuÉhÉïï qÉ×SÒ xÉU£ü AéåwÉ-cÉÉåwÉ-SÉWû Increases rapidly
mÉÏiÉ, U£ü, AÍxÉiÉuÉhÉï qÉ×SÒ xÉaÉlkÉ
accompanied by iÉ×whÉ-SÉWû-euÉU-xuÉåS Desire for cold vÉÏiÉÉæcNûÉ Intolerable to touch Appears first in middle part then spreads throughout body.
Table No. 2.6 Kaphaja Shotha:
cÉUMü92 xÉÑ´ÉÑiÉ93 uÉÉapÉOû94 MüTüeÉ vÉÉåjÉ
aÉÑ vÉÏiÉ ÎxlÉakÉ mÉÉhQÒû uÉhÉï or μÉåiÉ, MühQÒû, xÉÑÎmiÉ, aÉÑÂiuÉ Grows slowly Associated with pain, numbness, itching.
mÉÉhQÒû uÉhÉï UÉåqÉ, iuÉcÉÉ vÉÏiÉ ÎxlÉakÉ qÉ×SÒ ÎxjÉU, xsɤhÉ EwhÉÉæcNûÉ MüÌPûhÉ ÌlÉSì, uÉqÉlÉ, AÎalÉqÉÉlkrÉ After pressing the pit will not reappear in the night condition get aggravated. ÌlÉzÉuÉsÉÈ
aÉÑÂ
ÎxjÉU mÉÉhQÒû uÉhÉï, pÉÉåeÉlÉÉÌS mÉëÌiÉAÂÍcÉ
AÎalÉqÉÉl±, mÉëxÉåMü, ÌlÉSìÉÍkÉMü, uÉqÉlÉ mÉëuÉëÑ̨É
Takes longer time to appear and cure After pressing the pit will not reappear In the night condition gets aggravated.
Dwidoshaja shotha:
According to Vagbhata:
The causes of two doshas will have their respective symptoms appear in
simultaneously.
Anti Inflammatory effect of Devadaru 26
Disease Review
Table No. 2.7 Dvidoshaja
cÉUMü xÉÑ´ÉÑiÉ uÉÉapÉOû95 ̲SÉåwÉeÉ vÉÉåjÉ ---
---
Symptoms are not clearly mentioned but two SÉåwÉ symptoms represents present state.28
SANNIPATAJA SHOTHA
According to Charaka:
The shotha due to the combination of two doshas may be diagnosed by on the
basis of combined etiology, signs and symptoms. Similarly Sannipataja type of shotha
can also be diagnosed from the combinations of etiological factor .
According to Sushruta:
It is having symptoms of all the three doshas which will associates with colour
(Varna & Vedana) pain.
Table No. 2.8 xÉ̳ÉmÉÉiÉeÉ vÉÉåjÉÈ
cÉUMü96 xÉÑ´ÉÑiÉ97 uÉÉapÉOû xÉ̳ÉmÉÉiÉeÉ All symptoms represents after
the combination of all three SÉåwÉ s.
All symptoms represents after the combination of all three SÉåwÉ s along with discoloration and pain.
---
RAKTAJA SHOTHA
According to Sushruta:
All the symptoms will be similar to the pittaja shotha and which represent the
raktaja shotha but will be more blackish in colour31.
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Disease Review
Table No. 2.9 U£üeÉ vÉÉåjÉÈ
cÉUMü xÉÑ´ÉÑiÉ98 uÉÉapÉOû U£üeÉ
---
All symptoms like ÌmɨÉeÉ but it will be more blackish.31
---
ABHIGHATAJA SHOTHA
According to Vagbhata:
Abhighataja is that, which is caused by cutting, splitting, hitting etc. by sharp and
other kinds of weapons, by snow and cold breeze, touch by the juice of Bhallatak, hairs
of Kapikacchu, and sharp spikes (of grains etc.) shotha spreads from place to place is
very hot to touch, resembles blood in colour and usually having symptoms of pitta32.
Table No. 2.10 AípɱÉiÉeÉ vÉÉåjÉÈ
cÉUMü xÉÑ´ÉÑiÉ99 uÉÉapÉOû100 AípɱÉiÉeÉ
--- ÌmɨÉ, U£üeÉurÉ aÉÉåjÉsɤÉhÉ
Swelling spreads from place to place symptoms like ÌmɨÉeÉ present.
VISHAJA SHOTHA
According to Vagbhata:
Vishaja (caused by poison) is that produced by crawling or urinating over the
body, injuries by the tusks, teeth or claws of poisonous animals or even by the contact of
the excreta, urine, semen or cloths of even non poisonous animals, touch of poisonous
trees, wind (gas, smoke, fumes of poisonous nature) and rubbing of artificial poisons etc.
Anti Inflammatory effect of Devadaru 28
Disease Review
such a shotha is sof, movable, drooping down, quick to manifest and causing burning
sensation and pain.
Table No. 2.11 ÌuÉwÉeÉ vÉÉåjÉÈ
cÉUMü xÉÑ´ÉÑiÉ uÉÉapÉOû101 ÌuÉwÉeÉ
--- ---
Quick to manifest qÉ×SÒ cÉsÉ SÉWû vÉÔsÉ AkÉÉåaÉqÉlÉzÉÏsÉ (AuÉsÉqoÉÏ)
According to Madhava Nidana – Vishesha lakshana
Vataja – Vishamam pachyata, No particular time for ripening.
Pittaja – Achira – ripens quickly
Kapahja – chiram – slow process of ripening.
Three stages of Vranashadha (inflammation)
Amashotha lakshana – Mando shmata, Alpa shotha, katinyata, Twak savarnata, Manda
vedana.
Pachyamanashotha lakshana – There is a violent pain as that of pricking by needle,
Burning or cauterizing, Pricking by knife, scorpionor, Ant-bite like the patient will be
restless irrespective of position, the tumor gets elevated like blown leather bag, the skin
becomes pale, there will be fever, heat, thirst & loss of appetite.
Pakwa shotha lakshana – In pakwa condition pain relaxes, witish skin, Diminished
swelling, wrinkles appear on the skin, occasional itching.
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Disease Review
Sushruta and Madhava are of the opinion that in shotha there is involvement of all
the three doshas. Ruja is because of vata, Paka is because of pitta and puya is because of
kapha.
SADHYASADHYATA102
Before going to start the chikista of a particular disease, one should know about
the sadhyasadhyata of a disease, i.e. whether it is easily curable, with efforts or incurable
etc should be known. According to prabhava, the diseases are classified as sadhya and
asadhya. Sadhya is subdivided a sukha sadhya and krichra sadhya where as asadhya is
subdivided as yapya and pratyakhya.
If the rogi is krisha or Durbala or if associated with upadravas, when it moves to
the marma sthana, ruja yukta and associated with srava and sarvangashotha is considered
to be asadhya. Where as in aheenamamsa, ekadoshaja, nava, balavan vyakti shotha is
sukha saadhya.
UPADRAVA
Chardi, trishna aruchi,swasa, jwara, atisara,dourbalya, pipasa, hikka, kasa are the
updravas of shotha.
CHIKITSA SOOTRA103
Depending on bala, dosha and kaala, one has to see the nidana, dosha, rutu and
viparita chikitsa has to be done.
CHIKITSA104
Samanya chikitsa
1. Amavastha - langhana, pachana
2. Prakupitavastha – Vamana, Virechanadi vishodhana
3. Shotha in shira pradesha- shiro virechana
Anti Inflammatory effect of Devadaru 30
Disease Review
4. Shotha in urdhwa bhaga – vamana
5. Shotha in Adhava pradesha – virechana
6. Shotha because of snehapana – Rukshakarma
7. Malavibandhata in vataja shotha – Niruha basti.
Oushadhis used in Shotha
1. Gandiradyarishta
2. Astashataarista
3. Punarnavadyarishta
4. Phalatrikaadyarishta
5. Kshragutika
6. Kamsaharitaki
7. Chitrakaghrita.
8. Dashamoola kwatha
9. Abhayadhi kwatha
10. Shothari choornam
PATHYAPATHYA105
Pathya
Kulatha yusha, Trikatu, Yavakshara choorna, Mudga, Jangala pashu pakshi
mamsa, Koorma, Shiki, Shallka mamsa rasa, Sauvarchala, Grinjana, Patola, Vayasi,
Moolaka, Nimba, one year old Yava and Purana Shaali.
Apathya
Gramya, Jaleeya, Anupa mamsa, Lavana, Shushka, Navanna, Gouda (Guda
Padartha), Pishtanna, Dadhi, Tila, Madya, Amladravya vallura, Samashana,
Guru,Asatmya, Vidahi anna, Divaswapna and Maithuna.
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List of Single Drugs used as Shothahara.
Bilwa Agnimantha Jayanti
Shyonaka Pathala Punarnava
Kashmarya Prashniparni Harenuka
Shalaparni Brahati Apamarga
Kantakari Gokshura Twak
Shunti Patha Ela
Rasna Yashti madhu Tejapatra
Patola Rakta chandana Nagakeshra
Daru haridra Chitraka Indrayava
Nirgundi Apamarga Pippali
Bringaraja Eranda Danti
Priyangu Kushta Maricha
Vacha Chavya Ajamoda
Haridra Moolaka Katphala
Karkata shringi Katphala Pamakashata
Hingu Manjistha Kokilaksha
Nimba Guggulu Grinjanaka
Guduchi Kapitha
Jeeraka Paribhadra
Kulaththa Ashwatha
Amra Balataka
Haritaki Amalaki
Bibitaki Dathoor
Anti Inflammatory effect of Devadaru 32
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REVIEW OF INFLAMMATION
DEFINITION:
Inflammation is defined as the local response of living mammalian tissues to
injury due to any agent. It is a body defense reaction in order to eliminate or limit the
spread of injurious agent as well as to remove the consequent necrosed cells and
tissues.
HISTORICAL BACKGROUND
The features of inflammation were described in an Egyptian paper around
3000 BC. celsus, a Roman writer of the first century AD listed the four cardinal signs
of inflammation, they were rubor (redness) tumor (swelling), calor (heat) and dolor
(pain). These signs are more prominent in acute inflammation than in chronic
inflammation. Later Virechow added the fifth sign of functiolaesa (loss of function).
Inflammation is not a disease but a non-specific response that has a saluton
effect on its host, this obvious fact was noticed by the Scottish surgeon John Hunter in
1793.
Julius Cohnheim (1839-1884) who provided one of the first and best
microscopic description of inflammation and observed inflamed blood vessels in thin
and transparent membranes such as in the mesentery and tongue of frog. Noting the
initial vasolidation and changes in blood flow, the subsequent oedema caused by
increased vascular permeability and the characteristic leukocyte emigration.
Elie Metchnikoff, a Russian biologist in 1882 discovered the process of
phagocytosis by observing the ingestion of rose thorns by amebocytes of starfish
larvae and of bacteria by mammalian leukocytes and concluded that the purpose of
inflammation was to bring phagocytic cells to the injured area to engulf invading
bacteria. Metchnikoff contradicted the prevailing theory, that the purpose of
Anti Inflammatory effect of Devadaru 33
Disease Review
inflammation (humoral theory of immunity) was to bring in factors from the serum to
neutrilize the infectious agents. It became clear that both cells (phagocytes) and serum
factors (antibodies) were critical for defense against micro-organisms, this
strengthened by the discovery of the antitoxins by Behring and Kitasato (1890)
On the basis of simple experimental studies of inflammatory response on skin.
Sir Thomas Lewis established the concept that chemical substances such as histamine
locally induced by injury, mediate the vascular changes of inflammation, this
fundamental concept underlies the important discoveries of chemical mediators of
inflammation and the use of anti-inflammatory agents.
CAUSES OF INFLAMMATION
The agents causing inflammation are
1. Physical agents like heat, cold radiation, mechanical trauma.
2. Chemical agents like organic and inorganic poisons
3. Infective agents like bacteria, viruses and their toxins
4. Immunological agents like cell mediated and antigen antibody reactions.
Thus, Inflammation is distinct from infection- the former being a protective
response by the body while the latter is invasion into the body by harmful microbe &
their resultant ill effects by toxins.
Inflammation involves two basic proceses
• Inflammatory response
• Healing
Though both these processes generally have protective role against injurious
agents. Inflammation and healing may cause considerable harm to the body as
well. Ex: Anaphylaxis to bites by insects or reptiles, drugs, toxins, atherosclerosis
chronic RA, fibrous bands & adhesions in intestinal obstruction.
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SIGNS AND SYMPTOMS
The Roman writer Celsus described four cardinal signs of inflammation as
(a) Rubor (Redness): An acutely inflamed tissue appears red due to dilatation of
small blood vessels within the damaged area.
E.g., Skin affected by sunburn, cellulites by bacterial infection etc.
(b) Calor (Heat): Increase in temperature is seen only in peripheral parts of the
body such as skin. It is due to increased blood flow (hyperaemia) through the
region resulting in vascular dilatation and delivery of warm blood to the area.
E.g., Systemic fever.
(c) Tumor (Swelling): Swelling results from oedema, the accumulation of fluid in
the extra vascular space as part of the fluid exudates and to a much lesser
extent, from the physical mass of the inflammatory cells migrating into the
area.
(d) Dolor (Pain): Pain is the best-known feature of acute inflammation. It results
partly from stretching and distortion of tissues due to inflammatory oedema
and in particular from pus under pressure in an abscess cavity. Chemical
mediators like bradykinin, prostglandins and serotonin are known to induce
pain.
(e) Loss of function (Functio laesa): Movement of an inflamed area is consciously
and reflexly inhibited by pain, while severe swelling may physically
immobilize the tissues.
CLASSIFICATION OF INFLAMMATION
Inflammation may be classified on the basis of various factors.
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I) Based on duration & severity
Depending upon the defense capacity of the host & duration of response,
inflammation can be classified as acute & chronic.
Acute inflammation – It is of short duration & represents the early body reaction &
is usually followed by repair.
The main features of acute inflammation are –
1) Accumulation of fluid & plasma at the affected site.
2) Intravascular activation of platelets.
3) Polymorphonuclear neutrophils as inflammatory cells.
Chronic Inflammation – It is of longer duration & occurs either after the causative
agents of acute inflammation persists for a long time or the stimulus such that it
induces chronic inflammation from the beginning.
The characteristics features of chronic inflammation is presence of chronic
inflammatory cells such as lymphocytes, plasma cells & macrophages.
II) Based on the Nature of exudates
• Serous
• Fibrous
• Haemorrhage
• Purulent
• Catarrhal
III) Based on causative factors
• Tubular
• Syphilitic
• Staphylococci
• Foreign body reaction
• Allergic
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I. ACUTE INFLAMMATION:
a) CATARRHAL ACUTE INFLAMMATION:
This is confined to mucous membrane, the mucous cells of the lining and of
the mucous glands secrete large quantities of mucin, there is molecular desquamation
of the surface lining, not so pronounced as to appear as ulceration. The discharge on
the surface or in the lumen consists of mucous plasma, leucocytes and desquamated
epithelial cells, it is mucoid in the early stages and becomes mucopurulent later.
Acute catarrhal inflammation is mildest form of inflammation, but in some organs it
can progress to termination and can become chronic. E.g. Rhinitis of common cold,
catarrhal bronchitis.
b) FIBRINOUS OR SEROFIBRINOUS INFLAMMATION:
This is seen in the serous membranes, the pericardium, pleura, peritoneum etc.
It consists of plenty of fibrin in the exudates derived from the exudate plasma,
irrespective of the nature of the irritant, they react in a stereotyped manner.
Neutrophils and macrophages are seen in the fibrinous network.
c) SUPPURATIVE OR PURULENT INFLAMMATION:
This type is characterized by the formation of pus. In solid tissues and organs
suppurative inflammation causes Abscesses, in contrast to the circumscribed affection
in abscess formation the process may become diffuse and spreading. Diffuse lesions
in the connective tissue are described as “Phlegmonous Inflammation or Cellulites”.
d) ACUTE HAEMORRHAGIC INFLAMMATION:
In certain cases, bacterial toxins produce intense injury to the capillary wall
and allow large number of Red Blood Corpuscles to escape, making the exudates
haemorrhagic. E.g. In Influenza Pneumonia, Acute Glomerulonephritis etc.
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e) PSEUDO MEMBRANOUS INFLAMMATION:
This form of inflammatory reaction is characterized by the formation of a
membrane usually made up of precipitated fibrin, necrotic epithelium and
inflammatory white cells. The reaction is encountered only on mucosal surfaces
commonly in the Pharynx, Larynx, Respiratory passage etc. The membrane formation
results from an acute inflammation response to a powerful necrotizing toxin, out
pouring of exudates traps the necrotic and cellular debris producing a dirty gray-
white, rubbery membrane on the eroded surfaces. E.g. In Diphtheria.
f) ALLERGIC INFLAMMATION:
In this, Inflammation is primarily and exclusively by antigen-antibody
reactions. The injury in this is due to the occurrence of antigen-antibody union on
walls of the tissue cells, hypersensitivity has much greater significance. The vascular
changes are associated with a cellular exudates consisting of neutrophils, eosinophils,
plasma cells and macrophages. Eosinophils may be spectacular components, tendency
to necrosis and tissue decay due to accelerated reaction and increase in the Phagocytic
power of the Leucocytes with increase of eosinophils are distinct features in allergic
inflammation.
2. CHRONIC INFLAMMATION
The acute inflammatory response is unable to remove or neutralize an
injurious agent; the response is modified to chronic. It is not usual for a chronic
response to last many months but years. As the inflammatory process continues, fluid
exudates diminishes and cellular response assumes dominance, the chronic response
is dominated by a massive build up of cells in the affected tissue. These cells are
primarily macrophages and lymphocytes. In chronic inflammation the agent and the
host are just capable of resisting each other. The agents involved are of low inevitable
Anti Inflammatory effect of Devadaru 38
Disease Review
ability. They are unable to penetrate deeply in to or spread throughout the body of the
host. Such agents may be bacteria, fungi, larger parasites. Foreign bodies which are
insoluble in body’s fluid can also elicit a chronic inflammatory response.
Regardless of the specific nature of the inciting agent, its presence in the tissue
promotes a long term conflict with the phagocytic cells of the host; heavy infiltration
by the inflammatory cells progressively interferes with normal function. When the
process continues over a month and years, the function detoriates as tissue is
destroyed, accumulating inflammatory cells replace functional tissues and scarring
develops. This deterioration ultimately leads to somatic death.
TYPES OF CHRONIC INFLAMMATIONS
Following Four types are included in Chronic Inflammation:
1) Chronic Diffused Inflammation
2) Chronic Suppurative Inflammation
3) Chronic Granulomatous Inflammation and
4) Chronic Fibrinoid Inflammation.
1) CHRONIC DIFFUSED INFLAMMATION:
Exudates, which may be diffused or focal shows lymphocytes, plasma cells
and macrophages, under certain stimuli macrophages develop into epitheloid cells and
multinucleated giant cells. Fibroblasts are present, in older lesions fibrosis
conspicuous. E.g. Chronic Ulcer.
2) CHRONIC SUPPURATIVE INFLAMMATION:
It is a non-specific inflammatory cell infilteration, in which infiltration by
polymorphs and abscess formation. E.g. Actinomycosis
Anti Inflammatory effect of Devadaru 39
Disease Review
3) CHRONIC GRANULOMATOUS INFLAMMATION:
It is characterized by the formation of Granulomas, a tiny lesion composed of
epithelial cells and lymphoid cells at the periphery, also granulomas may have giant
cells, necrosis and fibrosis. It is seen in specific infective granulomas as in
Tuberculosis, syphilis. Leprosy etc.
4) CHRONIC FIBRINOID INFLAMMATION:
It is a degenerative phenomenon like rheumatoid arthritis, reheumatic fever etc.
TABLE NO 2.12 Differences between acute inflammation & chronic
inflammation
Acute inflammation Chronic Inflammation
1.Duration: Usually for days or weeks 1. Duration: For months or Years
2. Cardinal Signs: Present 2. Cardinal Signs: Doubtful or not
perceptible
3.Vascular Changes: Present 3.Vascular Changes: Not Marked
4. Exudation of Plasma: Present 4. Exudation of Plasma: Doubtful or
Absent
5. Cellular Exudates:
Neutrophils initially lates Macrophages and
Fibroblasts Stage of repair Lymphocytes
are few.
5.Cellular Exudates:
Histocytes Plasma cells lymphocytes
Fibroblasts are present Neutrophils
absent or very less in numbers.
7. GENERAL MECHANISM OF INFLAMMATION
The starting point of inflammation is the cell damage, living or inert, the cells
which do not damage are not capable of producing inflammation. However once the
damage has occurred the reaction takes place inevitably and proceeds through a
definite series of events to its ultimate end, i.e. repair of damage and restoration of
function.
Anti Inflammatory effect of Devadaru 40
Disease Review
GENERAL MECHANISM OF INFLAMMATION
• Vascular phenomenon changes
Vasodilation
Active hyperemia
Capillary dilation
Static of blood
Sludging of red cells in the capillaries
Pavementation of leukocytes
Exudation of fluid and out pouring of polymorphs
• Cellular response
Local
Exudation
Fluid of exudation
Cells of the exudation
General response
Fever degeneration
Leukocytosis
• Repair of tissues
Degenerative
Albuminous degeneration
a. Repuls degeneration
b. Healing cloudy swelling
c. Regeneration
Anti Inflammatory effect of Devadaru 41
Disease Review
Fatty degeneration
a. Suppuration
b. Abusers
c. Boil
d. Carbuncle
e. Cellulites
Proliferative
Phagocytes
a. Attachment
b. Engulfment
(i) Azophil
(ii) Special groused
c. Killing and degeneration
(i) Oxygen dependent mechanism
(ii) Oxygen independent mechanism
Cells included in the inflammatory exudates are :
• Neutrophil
• Eosinophils
• Mast cells
• Lymphocytes
• Plasma cells
• Macrophages
Anti Inflammatory effect of Devadaru 42
Disease Review
MECHANISM OF INFLAMMATION -
Management of inflammation and action of non-steroidal anti-inflammatory drug.
Irrespective of the nature of causative factors or the type of inflammation, the
tissue reaction in first few hours is stereotyped and similar. Its pathology can be
understood in the fallowing steps.
1.Vascular phenomenon
2.Cellular phenomenon
3.Repair
1.Vascular phenomenon:
Following changes will occur in vascular phenomenon one by one
i. Vasodilatation: Proceeded by transient vasoconstriction
ii. Active hyperemia
iii. Capillary dilatation
iv. Stasis of Blood
v. Sludging of red cells in the capillaries.
vi. Pavementation of leukocytes.
vii. Exudation of fluid and out pouring of polymorphs.
There are number of cells present in the inflammatory exudates which perform
various functions. Those are
a. Neutrophils
b. Eosinophils
c. Mast cells
d. Lymphocytes
e. Plasma cells
f. Macrophages
Anti Inflammatory effect of Devadaru 43
Disease Review
A brief description and the role is as follows.
a) Neutrophils: Neutrophils or Polymorphs are the cells along with Basophils and
Eosinophils are known as granulocytes, due to the presence of granules in the
cytoplasm, contains substances like proteases,myloperoxidase and alkaline
phosphates. Neutrophils are actively motile, get collected arround blood
vessels and passes through the tissue by active amoeboid movements, there
from the first line of defense in bacterial infections.
b) Eosinophils: These are larger than the Neutrophils and constitute 2-4% of the
total blood leucocytes. They appear only at the sites of inflammatory exudates
of diseases of immunological origin. They remain in the circulation for a short
peroid and rapidly attracted in the tiisues by the raised concentration of
released histamine. Eosinophils are phagocytic in nature. These may share
many structural and functional similarities with neutrophils, like their
production in the bone marrow, locomotion, lobed nucleus and presence of
granules in the cytoplasm. Granules of eosinophils are rich in
myeloperoxidase than neutrophils and lack lysozyme. High level of steroid
harmone (eosinopenia) leads to fall in number, and even disappear from the
blood. These may be increased in certain conditions like Allergy, Parasitic
infestations, skin diseases and certain malignant lymphomas.
c) Mast cells: These cells contain coarse basophilic granules in the cytoplasm
and a polymorphous nucleus, These granules are laden with heparin and
histamine. The functions of mast cells in normal Human being is not vivid.
They are believed to produce the acid.
d) Plasma cells: These are larger than the lymphocytes with more abundant
cytoplasm and an eccentric nucleus. These cells are normally not seen in
Anti Inflammatory effect of Devadaru 44
Disease Review
peripheral blood. They develop from lymphocytes and are rich in RNA and
Gama-globulin in their cytoplasm. There is an inter relationship between
Plasmocytosis and Hyperglobulinaemia. These cells are most active in
antibody synthesis. The number will increase when prolonged infection with
immunological responses. e.g. Syphilis, Rheumatoid Arthritis, Tuberculosis,
Hypersensitivity states and multiple myeloma.
e) Macrophages: These are large mono-nucleated cells play an important role in
the stages of Acute and Chronic Inflammations. It is believed that many
lymphocytes derived from the blood are converted in to microphages at the
site of inflammation, by increase in cytoplasm and enlargement of the nucleus
and are derived from Kuffer cells of the liver and histocytes. They form the
scavenger cells of inflammation, combine to form giant cells and need
phagocytic action. The giant cells are mainly of :
i. Tumour Giant Cells
a. Anaplastic Cancer Giant Cells
b. Reed-Sternberg Giant Cells and
c. Giant Cells of Tumour
ii. Foreign Body Giant Cells.
i. Tumour Giant Cells: It is of fallowing types
a. Anaplastic Cancer Giant Cells:
These are larger and have numerous nuclei which are hyper chromatic and
vary in size. These giant cells are not derived from macrophages but are formed from
dividing nuclei of the neoplastic cells.
Anti Inflammatory effect of Devadaru 45
Disease Review
b. Reed-Sternberg Giant Cells:
These are malignant tumour giant cells , which are binucleate and are seen in
various histologic types of Hodgkin's lymphomas.
c. Giant Cells of Tumour:
These cells are usually found in the bones, uniform distribution and
osteoclastic giant cells spread in the stroma.
ii. Foreign Body Giant Cells:-
These contain numerous nuclei, which are uniform in size and shape and
resemble the nuclei of macrophages, these nuclei are scattered throughout the
cytoplasm, these are usually seen in the chronic infective granulomas.
2.CELLULAR RESPONSE:
Cellular response can be explained in to a) Local response and b) General
response. The local response starts with the pavementing and emigration of
leukocytes before the cells of the damaged tissue release some chemicals that bring
about all the changes. The Vasodilation and increased permeability is due to the
substances like "leukotoxin" and "histamines" are produced by the damaged tissue
cells.
These stimuli activate both Hematogenic and Histogenic cells, which carry out
various functions like vascular phenomenon, pavementation and emigration of
leukocytes and various other cellular responses.
Following a local injury, there is a transient constriction in the vessels that
cause local Ischemia. This mommentary constriction is followed by an active phase of
hyperemia with dilation of vessels, this dilation chiefly occurs in arteries and venules
and at last in the capillary bed. The active hyperemia lasts for a few hours. The
capillaries get changed and become prominent.
Anti Inflammatory effect of Devadaru 46
Disease Review
The blood vessels keep on dilating and the active hyperemia is fallowed by the
stagnation of blood, which is termed as stasis and the clotting takes place in the
vessels. The blood supply to the tissue is lost and necrosis sets in the vasodilation that
follows the transient vasoconstriction (due to neural reflex) It is recognized that a
sensory fibre has a vasodilator branch to an arteriole. When there is an injury, there is
a reflex vasoconstriction and thus vasodilation sets in.
The vasodilation occurs under the influence of chemical mediators also, it was
postulated by Lewis (1927) that "H" like substance cause vasodilation. Further
Menklin postulated about "Leukotoxin". In addition, it increases the vascular
permeability and responsible for the emigration of leukocytes, the slowing of blood
flow in the vessels may be attributed to swelling of the endothelial lining of the blood
vessels, vasodilatation that decreases the pressure. Loss of blood fluid in interstitial
spaces makes the blood viscous. There is sludging of red cells. The red cells become
sticky and adhere to one another in masses and to the walls of the vessels.
In this slower blood stream, rearrangement of the corpuscles takes place, under
normal condition, the red and white cells flow intermingled in the central part of the
vessels forming an axial stream, which is separated from the wall by a clear plasmatic
zone free from cells. When there is some degree of injury, the leukocytes fall out of
the axial stream and come to occupy the plasmatic zone adhere to the vessel wall and
seem to drag themselves along with difficulty. In this way, the inner wall of the
capillary becomes paved by a broken line of leukocytes without the admixture of a
single red blood cell. This arrangement is called pavementing of leukocytes.
Normally the endothelial cells of the blood vessels and blood cells repel one
another due to change in the electrical potential, where these carry negative charges
with them, hence the repulsion. The endothelium becomes positvely charged and the
Anti Inflammatory effect of Devadaru 47
Disease Review
leukocytes are the first of the cellular elements to be attracted to and adhere to the
lining of the vessel.
The endothelial cells also become enlarged, proliferated and thus assume
round shape. The inter-endothelial space widens and through these spaces leukocytes
emigrate.
A) EXUDATION:
After dilation of blood vessels, the solid and fluid contents of plasma as well
as of the blood cells pass through the vessel walls and constitute within the tissues.
Thus, the fluid is rich in protein contents and the cells constitute the exudates.
B) FLUID OF THE EXUDATE:
Normally the walls of the blood vessels are permeable to the fluid, some ionic
salts and the molecules with molecular weight less than 10,000 Daltons, large part of
the fluid get reabsorbed and the remaining is carried by lymph channels.
But during inflammation, this exudate fluid, which originates from plasma
differs from it in several aspects. Its solid contents are almost double than the contents
of the lymph. Its specific gravity is 1.020. The main reason is that serum albumin and
serum globulin is present in exudate. The fluid molecules come out of vessels due to
increased permeability of vessels.
Besides this protein, the exudate contains various extractions like Urea, fibrin
forming elements, mucin ferments and immune bodies, oxidases, lipases and trysin.
All type of immune bodies may be found including cytolysin, haemolysin,
bacteriolysin, agglutinins, opsonins and complement fixing bodies. The formats and
the immune substances are distinctly higher in oedema than oedema produced due to
other causes.
Anti Inflammatory effect of Devadaru 48
Disease Review
FUNCTION OF FLUIDS OF EXUDATE :
1. It dilutes the soluble poisons and irritates, thereby reduces their direct effect.
2. It provides over runs of escape for the metabolites which are formed in excess.
3. It maintains normal hydrogen concentration.
The protolytic enzymes serve to complete the solution of the tissues which
have been injured or killed, thus aid in their removal. Exudate is rich in fibrin forming
proteins. The environment in which it is present favours fibrin formation, this serves
as the limits of extent of the inflammatory process. The fibrin mesh in the lymphatics
serve as a filter and with solid materials especially bacteria, if it is not dissolving by
protolytic enzymes it provides a frame work on which connective tissue grows and
healing takes place.
C) CELLS OF THE EXUDATES:
After pavementing the leukocytes emigrate in extra vascular spaces, as they
emerge from the outer margin of endothelium, a new basement membrane forms
between them and the endothelium disappears permitting release of the leukocytes in
to the extra vascular space without leaving any defect behind them, under the
influence of various chemical mediators, this phenomenon is known as "Chemotaxis".
D) PHAGOCYTES:
Phagocytes can be resolved in to three distinct ways
1. Attachment of the Particle to the surface of the phagocyte.
2. Engulfment.
3. Killing and degeneration of the ingested microbe or particle.
Anti Inflammatory effect of Devadaru 49
Disease Review
1. ATTACHMENT OF THE PARTICLE TO THE SURFACE OF THE
PHAGOCYTE:
These cells are recognized and attracted to bacteria by chemotactic factors
released by bacterial products as well as by tissue proteins, in order to establish a
bond between bacteria and the cell membrane of phagocytic cells, the micro
organisms get coated with opsonins which are naturally occurring factors in the
serum.
The main opsonin present in the serum IgG opsonin, is the Fe fragment of
immunoglobulin G, antibody in the serum that coats the bacteria. C3b opsonin is the
fragment of completement, which is generated by activation of completement
pathway.
Lactins are carbohydrate-bonding proteins in the plasma, which bind to
bacterial cell wall. Receptors mediated attachment of opsonized bacteria has been the
recognization step of Phagocytosis.
2. ENGULFMENT:
Leukocytes are able to respond to opsonins for that they display leukocyte
binding sites, once an opsonin coated particle is bound to the surface receptors of the
phagocyte, the particle is readily engulfed. Binding of a particle to the phagocytic
membrane elicits the engulfment, the phagocytic membrane flows around the particle
to enclose it in a cytoplasmic phagosome. Granular appearing lysosomes that contain
destructive agents then merge with the phagosome membrane, thereby bringing their
contents in to contact with the particle. As lysosome merge with the phagosomes their
number within the phagocyte are reduced and the phagocyte is degenerated. If the
particle is too large to be easily engulfed i.e. a multicellular parasite. There may be
regurgitation of the granule contents in to the tissue spaces. The leukocytes attempting
Anti Inflammatory effect of Devadaru 50
Disease Review
to engulf this large surface experiences frustrated phagocytosis and releases toxic and
degradative substances that damage the basement membrane and the surrounding cells
and the matrix.
The neutrophil cytoplasm contains two types of granules Azusophil and
Specific granules. Lysosomes contain acid hydrolases, neutral proteases, cationic
proteins, lysozyme.
i) AZUSOPHIL:
These lysosomes contain acid hydrolases, neutral proteases, cationic proteins,
lysozyme.
ii) SPECIFIC GRANULES:
Which contain lysozyme and lectoferiin but no hydrolases or peroxides.
Macrophages also contain azusophil granule. The process of degranulation pour in to
the phagosome powerful enzymes which kill the bacteria by different mechanisms.
3. KILLING AND DEGENARATION:
The micro-organisms after being killed by antibacterial substances are
degraded by hydrolytic enzymes, their mechanism fails to kill and degrade some
bacteria.These are of mainly two types, Oxygen dependent and Oxygen Independent.
1. Oxygen dependent:
It is an important mechanism of microbicidal killing by the production of
reactive oxygen metabolites (O2 H2O2, OH, HOCL, HOL, HOBr) a phase of increased
oxygen consumption by activated phagocytic leukocytes in presence of NADPH
oxidase.The NADPH oxidase which is present in the cell membrane of phagosome
reduces oxygen to superoxide ion (O2).
2O2 NADPH 2O2 (superoxide anion)
2O2 + 2H─ H2O2
Anti Inflammatory effect of Devadaru 51
Disease Review
Suproxide is subsequently converted in to Hydrogen peroxide (H2O2) has
bactericidal properties, this bactericidal activity is carried out either enzyme
myeloperoxidase present in the granules of neutrophils and monocytes or the enzyme
myeloperoxidse acts on Hydrogen peroxide in the presence of halides (Chlorides,
Iodide, Bromides) to form hypophalous acid (HOCl ). Which is more potent
antibacterial agent than hydrogen peroxide.
Reactive oxygen metabolites are useful in eliminating microbial organisms
that grow within phagocytes.
2. OXYGEN INDEPENDENT:
This mechanism involves the release of substances that damage bacterial cell
walls, disrupt bacterial replication and produce a low pH within the phagosomes
resulting from accelerated glycolysis, Which may be directly toxic and may indirectly
aid the function of other enzymes.
b) GENERAL RESPONSE:
The general celleular respons may be Fever and Leukocytosis.
i. Fever:
Fever is one of the most prominent systemic manifestation, particularly in
inflammation associated with spread of organisms into the blood stream. The patient
may have high fever charecterised by dramatic swings in the temparatur. The origin of
the fever may be uncertain, although it may be caused by the release of bacterial
endotoxins. In addition interleukin – 1 (IL-), prevously described as endogeneous
pyrogen released from the leukocytes is an important mediator of hyper pyrexia. This
mediator is taken up by lymphatics from the site of imflammation, which is circulated
in blood stream. It is believed that IL-1 initiates fever by inducing the synthesis of
PGE2 in the anterior hypothalamas and stimulating thermoregulatory centres.
Anti Inflammatory effect of Devadaru 52
Disease Review
ii. LEUKOCYTOSIS:
Increase in the number of circulating white cell is another charecteristic
significance of acute and chronic inflammation. When the inflammation is deep and
the local symptomatology is either not observes or impossible to demonstrate, then
leukocytosis is of assistance in determining the severity of the infection and the
degree of the resistance offered by the body. This requires not only an absolute count
(i.e. the total number of white cells per mm) but also the relative number of each type
of leukocytes particularly the number of neutrophils. In making the differential count,
the number of each kind of white cells in hundred is counted.
• A high absolute count (T.L.C) with a high neutrophil percentage indicate
severe infection and good body resisitance.
• A high absolute count with a moderate neutrophil percentage indicates a
moderate infection and good body resisitance.
• A low absolute count with high neutrophil percentage indicates severe
infection and weak resisitance of the body.
• All inflammatory states do not evoke neutrophilic leukocytosis. Infectious
mono nucleoses, whooping cough, mumps, rubella and undulent fever
charecteristicaly produce lymphocytosis.
Allergic inflammatory reaction like hay fever, bronchial asthama and parasitic
infection typically elicit eosinophilia. Some infections may cause leukopenia instead,
like infections caused by viruses, rickettsiae, protozoa and salmonelloses.
C. TISSUE CHANGES OR REPAIR:
There are two types of tissue changes
a. Degenerative
b. Proliferative.
Anti Inflammatory effect of Devadaru 53
Disease Review
a. DEGENERATIVE:
The two most common degenerations are
1. Albuminous degeneration or cloudy swelling
2. FATTY DEGENERATION
1. Albuminous degeneration or cloudy swelling:
It is closely related to hydrophic or vascular degeneration. Being manifestation
of a disturbance of protein metabolism, is called as Albuminous degeneration. It may
be caused by the bacterial toxins, chemical poison, malnutrition and other
disturbances.
The principle organs showing cloudy swelling are Kidneys, Liver and Heart
muscles. The organ affected is slightly enlarged owing to swelling of the cells of
which it is composed. It is pale as blood vessels being compressed by the swollen
cells. The cut surface has rather cloudy appearance and slightly opaque.
2. FATTY DEGENERATION:
Fatty degeneration or Fatty metamorphosis is a true sickness of cells caused
by some injurious influences. It is best seen in Liver, Kidney and Myocardium. The
fat metabolism is interferred with fat accumulations in the cell. In some cases there is
merely unmarking of fat already present. The causes of fatty degenerations are
• Poisons
• Anoxia
The organs look fatty. The liver and kidneys are pallor and softer than normal.
The heart is soft and flabby. Ultimately the tissue becomes necrosed.
If the irritant is intense, the effect is degenerative destruction. If it is mild, acts
as stimulant and leads to proliferation. At the centre of the inflammatory area the
action of the irritant is severe, degeneration predominates at the periphery and the
Anti Inflammatory effect of Devadaru 54
Disease Review
action is mild. The tissue may be stimulated to proliferation. thus this part of the
inflammation is known as repair or healing.
i) SUPPURATION:
If the dead tissue in an inflammed area undergoes softening and liquification is
known as the process of Suppuration, the fluid formed is called the Pus, by this
method the dead material is removed from the body.There are three requisites for
suppuration.
i. Necrosis
ii. Presence of sufficient leukocytes
iii. Digestion of the dead materials by protolytic fermentation.
If any one of these are absent suppuration does not occurs.The digestive
enzymes are produced mainly by the leukocytes to a lesser extent by the necrosed
tissue cells and the infecting bacteria. These are neutralized by anti enzymes present
in the serum. If there is less leukocytes or more serum liquification does not take
place.
ii. ABSCESS:
It is an example of a localized suppuration. The inflammation is limited to the
area and as the irritant is pyogenic, pus is produced. The cells in the centre of the
inflammatory area are killed and liquified by protolytic enzymes. In this way a cavity
is produced which contains pus. The wall of the abscess cavity consists of damaged
but still living tissues. Hence the spread of infection is limited, this limiting zone is
crowded with polymorph nucleus leukocytes and macrophages filled with debris. Pus
cells are continuously dicharged from this, thus the abscess is chronic or if the
infection is dying out, the macrophages will greatly outnumber the polymorphs
further out, the tissue become more and more normal.
Anti Inflammatory effect of Devadaru 55
Disease Review
If the infection is continuously active more and more material is added to the
abscess, So that the pressure within the abscess increases. Thus it points in the
direction of less resistance. If the abscess enters the muscle sheath, it may extent
along a considerable distance.
iii. BOIL:
It is an abscess of a Sebaceous gland or a hair follicle caused by the
Staphylococcus aureus, which has penetrated the opening of the duct. There is a
marked fibroblastic proliferation, which with intercellular formation of fibrin, causes
the characteristic indusation. The tension becomes high and causes pain. There may
be a very little liquification of the necrosed tissue, So that the centre of the boil is
composed of a solid "Core" instead of Pus.
iv. CARBUNCLE:
It is the infection spread to the subcutaneous tissue where it causes a more
diffused lesion which discharges on the surface by a series of openings. The pus
becomes inspected and the dead tissue is converted into a mass of fatty debris in
which lime salts may be deposited.
v. CELLULITIS:
When the suppuration spreads through the tissues, the condition is called
cellulitis. The fibrin that forms as a result of proliferation, inflammed part limit the
infection.
3. REGENERATION:
This implies to a complete renewal of the tissue as in liver. The process of
healing if fundamentally the same in all the wounds. It consists of two parts. Removal
of inflammatory material and necrotic debris, which may be more or little.
Anti Inflammatory effect of Devadaru 56
Disease Review
Replacement or reconstruction of the original tissue to a greater degree as much as
possible.
The repair involves the invasion and replacement of dying and dead tissue by
immature mesenchyma called Granulation tissue, which is a highly vascular tissue.
On account of its cellularity a granulating surface has a remarkable power of
resistance against bacterial infection. The granulation tissue grows to maturity from
below to up words. When the wound is aseptic the epithelium will grow in from the
edges as a delicate blue pellicles, gradually it becomes thick and opaque.
When the surface is covered by epithelium, the process of devascularization
begins. The new vessels, being no more needed will gradually disappear. The scar that
is red becomes white and bloodless106.
REVIEW OF ANTI-INFLAMMATION
Drugs which can normally be used to almost every type of inflammatory
conditions are known as anti-inflammatory drugs These have two major groups.
1. Steroidal anti-inflammatory drugs in the form of gluco corticoids.
2. Non-Steroid anti-inflammatory drugs (NSAID)
Mode of action of steroidal anti-inflammatory drugs
ACTH and Glucocorticoids prevent the clinical features of inflammation i.e.
local heat, redness pain and swelling. Their action is based on reducing the increased
permeability of capillaries and maintenance of the integrity of the cell membrane
even in the presence of toxins. Stabilization of lysosomes release from the
granulocytes by inhibiting phagocytosis. Also acts on fats phase of inflammation and
inhibits capillary proliferation deposition of collagen cicatrisation. But fibrous tissue
once formed is not dissolve by corticosteroids.
Anti Inflammatory effect of Devadaru 57
Disease Review
Hence the anti-inflammatory effect of steroidal therapy is non specific. The
steroid inhibit the phospholipase enzyme which is essential to activate the cell
membrane. This activation release the arachidonic acid, which metabolises to produce
inflammation. But once the chain is initiated it cannot be stopped by the steroidal
therapy, moreover in large doses, it may interface with wound healing.
9. CLASSIFICATION OF ANTI-INFLAMMATION
These are broadly classified into two groups. Narcotic Analgesics or opoid
analgesics and Non-narcotic analgesics or non opoid analgesic or NSAID, non
steroidal anti-inflammatory drugs.
1. NARCOTIC ANALGESICS:
These agents are capable of relieving severe degree of pain but are moderately
or strongly addicting. This group includes opoids which binds to the opoid receptors.
These, further classified in to Natural opium alkaloids ( e.g. Morphin)., Semi-
synthetic opiums (e.g. Diacetyle morphin or acetyle morphin) and Synthetic opoid
(e.g. Pethedine).
2. NON-NARCOTIC ANALGESICS OR NON OPOID ANALGESIC or NSAID:
In this the agents relieve mild to moderate degrees of pain and are considered
as non active. This group includes aspirin analgesic and other analgesics and
antipyretic drugs and these have no affinity for the opoid receptors, but the site of
action is only peripheral and further NSAID is divided in to Potent anti-inflammatory
and good analgesics, Potent anti-inflammatory and good analgesics, Moderate anti-
inflammatory and moderate analgesics and Poor anti-inflammatory and good
analgesics.
Anti Inflammatory effect of Devadaru 58
Disease Review
A. POTENT ANTI-INFLAMMATORY AND GOOD ANALGESICS:
i. Salcylates e.g. Aspirin
2. Oxy cum derivatives e.g. Paraoxicam.
B. POTENT ANTI-INFLAMMATORY AND GOOD ANALGESICS:
i. Pyrazolin derivatives e.g. Phenyl butazone.
ii. In dol derivatives e.g. Indomethacin.
3. MODERATE ANTI-INFLAMMATORY AND MODERATE ANALGESICS:
i. Propyonic acid derivatives e.g. Ibuprofen
ii. Anthranlic derivatives e.g. Mefenamic acid.
iii. Aryl acetic derivatives e.g. Diclofenac.
4. POOR ANTI-INFLAMMATORY AND GOOD ANALGESICS:
i. Para amono phenyl derivatives e.g. Paracetamol or acetaminoidene.
ii. Pyrozolon derivatives e. g. Metamezole.
10. MANAGEMENT OF INFLAMMATION AND ACTION OF NON-
STEROIDAL ANTI INFLAMMATORY DRUGS (NSAID)
As stated earlier, the activation of cell membrane releases arachidonic acid, it
is metabolized by cyclo-oxygenase pathway and produce prostaglandins (PGs).These
include PGG2, PGH2, PGl2, PHE2 and PGE2 and cause vasodilatation and potentiate
oedema. Some of these are supported to inhibit platelet aggregation.
These further sensitize the chemical receptors of the afferent pain endings to
other chemical mediators like bradykinin and histamine. Aspirin and asperin like
NSAID have been shown to inhibit release or synthesis of PG5 and thus produce
beneficial anti-inflammatory condition where PGs are synthesized locally. It is unable
to produce any analgesic effect where the sensory nerves are directly stimulated.
Anti Inflammatory effect of Devadaru 59
Disease Review
Some of the NSAID produce anti-inflammatory effect indirectly,like
indomethacin. It inhibits phosphodiesterase and thus increases the intracellular
concentration of cyclic ATP, Cyclic ATP has been shown to stabilize membrane
including lysosomal membrane in polymorphonuclear leukocytes. This prevent the
release of enzymes important in the inflammatory responses. Some drugs may inhibit
the activation of T-lymphocytes which release lymphokinase, which plays an
important role in mediating inflammation107.
Anti Inflammatory effect of Devadaru 60
Methodology
METHODOLOGY
Source of drug collection:
The genuine quality of setem bark of devadaru (cedrus devadaru) were
purchased from Alva pharmacy, Moodbidri, Dakshina kannada district. Botanist and
other experts verified the stem bark and its identification confirmed.
Preparation of drug:
Drying the stembark of devadaru:
The stembarks were dried completely under shade to obtain dry barks and also
to minimize the loss of volatile oil.
Powdering:
After proper drying the stembarks were subjected to powdering in pulvarizer
under mesh to get coarse powder and stored in air tight container.
Preparation of extracts:
Extraction of both Aqueous and alcohol extraction of devadaru was done in
Dravya guna department. PG cum Research center DGMAMC Gadag.
Preparation of alcohol extract: Drug- coarse powder of stem bark of devadaru108
We followed the continuous hot percolation process, Drug to extract is packed
in a cylinder made up of filter paper called as Thimble” and is placed in body of
sauxhlet extractor. The solvent is placed in flask apparatus is fitted. When the solvent
is boiling on heating the flask it gets converted to vapour. These vapours enter into the
condensor through the side tube and get condensed into hot liquid, which flak on the
column of the drugs. when extractor gets filled with solvent level of the siphon tube
also raises up to its top solvent containing active constituents of drug in siphon tube,
siphons over and run into the flask, thus emptying the body of the extractor. This
alteration filling and emptying the body of extraction goes on continuously. This
Anti Inflammatory effect of Devadaru 61
Methodology
process of filling and empting of extractor is repeated until the drug is exhausted,
normally process is repeated for 15 min for complete exhaustion of drug. Extraction
was done in three batches of these, the extraction process was carried out for about 18
hours to each batch. After the extraction the solvents were distilled off to obtain semi
solid extract & concentrated on magnetic stirrer the weights of each batch of extract
were recorded.
After the effective solvent were concentrated at room temperature in reduced
pressure using evaporator and extraction obtained was weighed its percentage was
calculated. The colour and consistency of extract was noted.
Thus obtained extract was subjected to preliminary phyto chemical
investigation and pharmacological screening for anti inflammatory activity by
carrageenan induced paw oedema method.
Preparation of Aqueous extract109
We followed the cold maceration method. One kg of coarse powder of
devadaru bark soaked in 5 ltr of chloroformed water (to prevent fungal growth) in
closed container for 24 hours, the mixture stirred continuously during first 6 hours and
allowed to stand for next 18 hours, Then the water was filtered completely to a tarred
flat bottomed dish and evaporated to dryness on a water bath. Dry for 6 hours cool in
a dissector for 30 minute. The solid extract thus obtained was weighted & stored in
the glass bottle sealed and kept in refrigerator.
Thus obtained extract was subjected to preliminary phytochemical
investigation & pharmacological screening for Anti inflammatory activity by
carrageenan induced paw oedema method.
Anti Inflammatory effect of Devadaru 62
Methodology
Preliminary Phytochemical investigations of extracts110
Qualitative chemical tests were conducted for alcoholic and aqueous extracts
of Devadaru (cedrus deodara) to identify the various phyto constituents. The various
tests and reagent used are given below and observation are recorded.
Material:
Drug: Aqueous & Alcoholic Extractive sample of Devadaru (cedus deodaru)
Equipments: Test tube, holder, stand, spirit lamp, pipette, glass rods, beakere 50 ml
to 250 ml, conical flask, water bath.
Methods
1) Test for sterols:
Salkowaski test A few drops of concentrated sulphuric acid was added to the 5
ml of sample solution (extract) shaken and allowed to stand and observed the lower
layer If it turns to red indicates the presence of sterols.
2) Test for Triterpenoids:
Salkowaski test : A few drops of 10 % concentrated sulphuric acid is added to the 5
ml of sample solution, shaken and allowed to stand (if lower layer turns yellow
indicates the presence of triterpenoids)
3) Test for Glycosides
Keller killiani test: The 5 ml of the solution with few drops of glacial acetic acid in 2
ml of ferric chloride solution and conc H2SO4 is added from the sides of test tube,
then observed for the separation between two layers, if lower layer shows reddish
brown & upper layer turns bluish green indicates the presence of Glycosides.
4) Test for saponins:
Foam test : Sample solution mixed with saponins and shaken, if there is formulation
of stable forth for one men it indicates the presence of saponins.
Anti Inflammatory effect of Devadaru 63
Methodology
5) Test for Lipids
Few drops of 0.5 N alcoholic potassium hydroxide is added to a small quantity of
extracts along with a drop of phenphthalain, the mixture is heated on water both for 1-
2 hour there is formation of soap or partial nutratization of alkali indicates presence of
lipids.
6) Test for carbohydrates
Benedict’s test: Test solution with Benedicts regent and boiled on water both if it
shows reddish brown precipitate.
7) Test for Alkaloids
Hager’s test: Sample solution with Hager’s reagent (saturated picric acid solution)
mixed & allowed to stand. If it gives yellow PPT indicates the presence of alkaloids.
8) Test for Flavonoids:
Ferric chloride test: Sample solution with few drops of Ferric chloride solution
mixed and allowed to stand. If it shows intense green colour indicates the presence of
Flavonoids.
9) Test for Proteins:
Xanthoproteic test: Sample solution treated with concentrated nitric acid and on
boiling if it shows gives yellow precipitate. It indicates the presence of proteins.
Million’s test: Sample solution is added with million’s reagent and heated on a water
bath.
10) Test starch
Anthrone test: Sample solution is added with Anthrone then boiled on water for 10
min. it shows greenish black colour it indicates the presence of stomach.
Anti Inflammatory effect of Devadaru 64
Methodology
11) Test for oils:
A small quantity of petroleum ether and benzene extract is pressed separately between
fitter papers if oil stains on the paper indicates is the presence of oils.
Physico chemical analysis of Devadaru
Determination of Foreign matter
100gm of the drug sample is taken and spread it out in a thin layer. The
foreign matter should be detected by inspection with the eye or by the use of lines
(6X) separated and weigh then calculated the % present.
Determination of Total Ash
About 3 gm of the bark powder of drug is taken in tared silica dish ignite it by
dreadyally increasing the heat to 500-6000C until it is white, indicating the absence of
carbon then it is cooled & weighed then calculate the %.
Determination of acid soluble ash
To the crucible containing the total ash add 25 ml of hydrochloric acid cover
with watch glass and boiled gently for 5 minutes collect the insoluble matter in a
cubicla or on an ashen filter paper wash with hot water and ignite calculate the % of
acid soluble ash with reference to the air dried drug.
Determination of water soluble ash
To the crucible containing the total ash, add 25 ml of water and boiled for 5
mins, then collect the insoluble matter in a crucible or on an ashen filter paper, wash
with hot water and ignite for 15 minutes at a temp not exceeding 4500C substract the
weight of the insoluble matter from the height of the ash. The difference in weight
represent the water soluble ash calculate the % of water soluble ash with reference to
the air dried drug.
Anti Inflammatory effect of Devadaru 65
Methodology
Determination of Alcohol soluble extractive
Macerate 5 gm of the air dried drug, coarsely powdered with 100 ml of
ethanol (Alcohol) of the specified strength in a closed flask for 24 hrs. shaking
frequency during the first 6 horus and allowed to stand for 18 hrs, thereafter, filter
rapidly, taking precaution against loss of solvent, evaporate 25 ml of the filtrate to
dryness in a tasted flat bottomed shallow dish, and dry at 1050 and weighed calculate
the percentage of Alcohol soluble extract with reference to the air dried drug.
Determination of water soluble extractive
Add 5gm to 50ml of water at 800 in a stopped flask, shaken and allowed to
stand for 10 mins cool add 2 gm of kieselghur and filter, transfer 5 ml of the filtrate to
a tared evaporating dish, 7.5 cm in diameter evaporate the solvent on a water bath,
continue drying for 30 mins finally dry in a steam oven for 2 hours and weigh the
residue calculate the percentage of water soluble extract with reterence of the air dried
drug.
Identification by T.L.C
Drug: Extraction of sample (Aq & Alc) which is treated with 1:10ml solute; solvent
like ethyl alcohol with dilution method.
Equipment: Silica gel, TLC kit, hot air oven, standard glass, wattaman glass plate,
beakers, sprayer.
Chemicals: Dragendroff’s reagent, Silica gel, ethyl alcohol.
Method: T.L.C. of the ethyl alcohol extract of the sample & Aqueous extract of the
sample was carried out as follows.
The silica gel powder mixed with water and made thin paste, then with the
help of glass slide, the silica gel was spread on glass plates uniformly, After some
times the air dried plate were kept in a hot oven at110-120 degree centigrade heay
Anti Inflammatory effect of Devadaru 66
Methodology
was given continuously then the prepared sample is kept on a side of the plate then
immersed in solvents upto 30 minutes then Dragendroff’s solution is sprayed on the
plates.
A parameter called the Rf value is always used in TLC this is determined as
follows.
Rf = Distance traveled by the solute
__________________________
Distance traveled by the solvent
Aq extract = 12.6 Alc extract = 12.5
_____ = 0.96 _____ = 0.86
13 14.5
Experimental study
Place of work:
The study was conducted in PG cum Research center D.G.M.A.M.C Gadag.
Preliminary phyto chemical investigations of Devadaru carried out at PG cum
Research center DGAMC Gadag source of animals.
Source of animals:
The required number of Healthy albino rats of either sex were selected for
experimental study and maintained in the animal house. In PG cum Research center
D.G.A.M.C. Gadag.
Housing and feeding of animals:
The animals were maintained at room temperature 250C, with 12 hrs day and
dark cycles, the standard laboratory diet was given with an unlimited supply of
drinking water.
Anti Inflammatory effect of Devadaru 67
Methodology
Preparation of animals:
The animals were randomly selected, marked to permit individual
identification and kept in their cages for one week prior to dosing to allow for
acclimation to the lab condition.
Preparation of doses/Vehicle
All the extracts were prepared as a suspension by triturating with distilled
water and with 1% tween20.
Mode of administration
Administration of drug through intra gastric tube using 2 ml disposable
syringe fitted with 20 gauze stainless steel needle provided with suitable smooth
catheter was used for drug administration to avoid injury to the rats.
Pre determined quantities of extracts were mixed with distilled water & 1%
tween 20 (calculated quantity) and suspension was prepared known quantity of
suspension was taken in the syringe & pushed directly.
Calculation of the dose
Rat dose = Human dose X 0.018 X 5
Trial drug: Aqueous extract
Alcoholic extract
20mg/100gm body weight – (Ref Indian journal of Pharmacology (1973) P.No-335)
Conversion of 1Kg body weight
Trial drug A – Aqueous extract - 20mg / 100gm body wt
200mg/Kg body wt
Trail drug B – Alcoholic extract - 20mg / 100 gm body wt
200 mg/ kg body wt
Standard drug
= Human dose X 0.018 X 5
= 1800mg X 0.018 X 5
= 32.4 X 5
= 162 mg / kg body wt
Anti Inflammatory effect of Devadaru 68
Methodology
Table 3.1 Protocol of experimental study
1 Sample 24 albino rats of either sex are selected randomly
2 Inclusive criteria Healthy albino rats weight – 150 – 200 gms
3 Exclusive criteria Other wise does not full fill above condition.
4 Groping Each group having 6 rats, kept in separate cage
Group I – Control group 1% normal saline was fed orally to the
albino rats at the dosage of 1 ml each animal in the single dose.
Group II – Standard group Ibuprofen suspension was fed orally
to the albino rats at the dosage of 100 mg/kg body weight.
Group III – Trial group A
Aqueous extract of devadaru is given at the dosage of 200 mg/
kg
Group IV – Trial group B
Alcoholic extract of devadaru is given the dosage of 200 mg/kg.
Table No 3.2 Concentration dose and duration before induction of inflammation
Group Drug or
extract
Dose Route of
administration
Time of
administration
prior to induce
inflammation
Control Group
I
1% Normal
saline
0.2ml /rat Orally 60 min
Standard
Group II
Ibuprofen 162mg/kg Orally 60 min
Trial group A
Group III
Aqueous
extract
200 mg/kg Orally 60 min
Trial group B
Group IV
Alcoholic
extract
200mg / kg Orally 60 min
Anti Inflammatory effect of Devadaru 69
Methodology
Procedure111
• Total 24 albino rats were taken for the experimental study and subjected them
in four groups of six rats in each group.
• One hour before inducing inflammation the prepared medicines were
administered orally to the respective groups of rats.
• Then inflammation is induced by injecting 0.1 ml carrageenan into the sub
plantar region of the left hind paw of all the groups.
• Paw volume of all the rats were measured after ½ hr, 1 hr, 2 hr, 3hrs. by using
plethymograph.
• Then compare the anti-inflammatory effect of aqueous & alcoholic extract of
Devadaru with control & standard drug treated groups.
Statistical analysis:
The data collected were statistically analyzed by using unpaired test, paired ‘t’
test – 4 ANOVA with the consultation of biostatistician.
Anti Inflammatory effect of Devadaru 70
Results
RESULTS
OBSERVATION AND RESULTS
Observation during Alcoholic extract of Devadaru [Cedrus deodara ]
Observation during Aqueous extract of Devadaru
Preliminary phyto chemical analysis of Devadaru
Physico chemical analysis of Devadaru
All the datas about the parameters considered for the study
Results are compared
Observation regarding the preparation of the drug
The dried stem barks of devadaru were brown in colour with characteristicof
aromatic odour. 2 kg of Devadaru [cedrus deodara] was taken. Out of that we
obtained 1980gms of dried devadaru The dried stem barkswere subjected to
powdering in the pulverizer.The final yield of coarse powder was about 1.8 kg
Observation during preparation of the Alcoholic extract
By appropriate technique the coarse powder of Devadaru is put in the round
fold of filter paper in sauxhlet apparatus. So that it cannot obstruct any path
ways of sauxhlet apparatus.and uniform temperature is maintained.
During each batch, the cycles were continued till up to extractive factors of the
powder were get completely extracted in to the solvent then and then only
every batch was stopped.
After extraction solvents were distilled off
Observation was done so that the solvent is completely distilled off from the
total extraction.
Semisolid extraction taken off and put over the magnetic stirrer for
concentration of extraction should not be so liquid or completely dried.
Anti Inflammatory effect of Devadaru 71
Results
500gm of coarse powder of Devadaru yielded about 50gm alcoholic extract
(10%) the alcoholic extract was dark brown in colour with aromatic odour.
Observation during Aqueous extract of Devadaru
200gm of coarse powder of Devadaru (cedrus deodara) yielded about 18gm of
aqueous extract. The aqueous extract was dark brown in colour with aromatic odour.
Observations of Preliminary Phytochemical Test:
1) Test for Sterols:
a) Salkowiski's test
Alc Extract + Conc H2 SO4 Shaken Lower layer turns red.
Indicates the presence of Sterols.
Aq Extract + Conc H2 SO4 Shaken Lower layer does not turns red.
Indicates the absence of sterols.
b) Sulphur test
Alc Extract + Sulphur Powder Shaken Sinks
Indicates the presence of Sterols
Aq Extract + Sulphur Powder Shaken does not Sinks
Indicates the absence of Sterols
2) Test for Triterpenoids:
Salkwoski's test:
Alc Extract+Conc H2 SO4 Shaken lower layer turns to red.
allow to stand
Indicates Presence of Triterpenoid.
Aq Extract+Conc H2 SO4 Shaken lower layer turns to red.
allow to stand
Indicates Presence of Triterpenoid.
Anti Inflammatory effect of Devadaru 72
Results
3) Test for Glycosides
Keller Killiani test
Alc Extract+ Glacial acetic acid in + Conc H2 SO4 No separation between two
2ml of ferric chloride
layers
Aq Extract+ Glacial acetic acid in + Conc H2 SO4 No separation between two
2ml of ferric chloride
layers
Indicates absence of Glycosides in both the extracts.
4) Test for Saponin's:
a) Foam test:
Alc Extract+Saponin Shake H2O No Formation of froth.
Indicate the absence of Saponin.
Aq Extract+Saponin Shake H2O No Formation of froth.
Indicate the absence of Saponin.
5) Test for Lipids
Alc Extract+0.5 N alc potassium + a drop of phenolphthalein heated on water bath for
1-2 hrs Shake H2O
formation of soap. Indicates the presence of lipids.
Aq Extract+0.5 N alc potassium + a drop of phenolphthalein heated on water bath for
1-2 hrs Shake H2O
formation of soap. Indicates the presence of lipids.
6) Test for Carbohydrates:
Benedict's test:
Alc extract + Benedict's reagent boil on water bath reddish brown PPT
Indicates the presence of Carbohydrate
Aq extract + Benedict's reagent boil on water bath reddish brown PPT
Indicates the presence of Carbohydrate
Anti Inflammatory effect of Devadaru 73
Results
7) Test for Alkaloids:
Acid soln of sample + Hager's reagent Picric acid Observed yellow PPT
saturated
Indicates the presence of Alkaloids in both extracts
8) Test for Flavonoids:
Ferric Chloride test
Alcoholic extract soln +Few drops of Ferric does not shows intense green
Chloride
colour.
Indicates absence of Flavonoid.
Aq extract soln +Few drops of Ferric does not shows intense green colour.
Chloride
Indicates absence of Flavonoid.
9) Test for Tannins:
a) 1 ml alcoholic soln treated with Fecl2 dark precipitate
Indicates presence of Tannin.
b) Alcoholic Soln treated with lead acetate white precipitate
Indicates presence of Tannin.
a) 1 ml Aq soln treated with Fecl2 dark precipitate
Indicates presence of Tannin.
b) Aq Soln treated with lead acetate white precipitate
Indicates presence of Tannin.
10) Test for Proteins:
Xanthoproteic test
Alcoholic extract soln +conc Nitric acid boiling does not shows Yellow PPT
Indicates absence of Proteins
Anti Inflammatory effect of Devadaru 74
Results
Aq extract soln +conc Nitric acid boiling shows Yellow PPT
Indicates presence of Proteins
11) Test for Starch:
Alcoholic extract soln +Anthrone boiling on shows Greenish black colour
Water bath
Indicates presence of Starch
Aq extract soln +Anthrone boiling on shows Greenish black colour
Water bath
Indicates presence of Starch
12) Test for Oils:
Oils stains on the filter paper.
Indicates the presence of oil in both the extracts.
Table No. 4.1
Results of Preliminary Phytochemical investigation of Devadaru (Cedrus
deodara)
Chemical Tests Alcholic extract Aqueous extract
Test for Sterols + -
Test for Triterpenoids + +
Test for Glycosides - -
Test for Saponins - -
Test for Lipids + +
Test for Carbohydrates + +
Test for Alkaloids + +
Test for Flavonoids - -
Test for Tannins + +
Test for Resins + +
Test for Proteins - +
Test for Starch + +
Test for Oils + +
Anti Inflammatory effect of Devadaru 75
Results
Table No. 4.2
Physico chemical values of Devadaru (Cedrus Deodaru)
Foreign matter 0.23 %
Total Ash 4.1 %
Acid soluble Ash 17.5%
Water soluble Ash 12.5%
Alcoholic soluble extractive 86%
Water soluble extractive 54%
Identification by TLC
About three to six centimeter solvent front migration is sufficient to effect proper
separation Wattman TLC plates produced from 4-5 micro-meter, Silica gel, with an
inert binder to form 200 mm layers about 7 cm development distance was achieved
sample preparation in TLC needs a concentrated solution as very less amount to be
applied and it had been developed using the technique of TLC.
The details of TLC as follows
Table No 4.3
Plate Size : 20 x 8 cm
Technique : One way ascending
Temperature : 30 C
Examination : Day light after spraying
Plate thickness : 3 mm
Activation temperature : 110 C
Time : 30 min- 1 hr
Detecting Spraying Reagent : Dragendroff's reagent
Absorbent Layer : Silica gel G(Activated) percolated plates
Solvent System : Chloroform
Anti Inflammatory effect of Devadaru 76
Results
• The Silica gel powder mixed with water and make thin paste ,then with the
help of glass slide the silica was spread on glass plate uniformly.
• After some times the air dried plates are kept in a hot oven at 110 C -120 C
heat was given continuously.
• For one hour then the prepared sample was kept on one of the plate then
immersed in a solvent up to 10 minutes and then Dragendroff's solution is
sprayed on the plates.
During this procedure following observations were observed:
• The Silica gel slurry taken on plates with the help of glass slide, the silica gel
was spread on glass plates uniformly.
• After sometimes the air dried plates were kept in hot oven at 110 C- 120 C.
heat was given continuously.
• After that, the prepared sample was kept inside the developing chamber with
the plate, then immersed in a solvents up to 30 minutes , closing the plate with
the lid.
• After Dragendroff's reagent was sprayed on the plates.
• Black spot was observed on TLC plate.
Results of TLC
Rf = Distance traveled by the Solute
Distance traveled by the solvent
Alc extract Rf = 12.5
= 0.86
14.5
Aq extract Rf = 12.6
= 0.96
13
Anti Inflammatory effect of Devadaru 77
Results
Observation of experimental study
Sample size
24 Albino rats were selected for the study
I. Inclusive criteria:
i) Healthy albino rats
ii) Albino rats weighing 150-200 gm
iii) Albino rats between 90-120 days old were included.
II) Exclusive criteria
i) Unhealthy Albino rats
ii) Weighing within 150 & above 200 gm
iii) Albino rats of below 90 days & above 120 days were excluded.
Induction method
The prepared medicines were administered orally to the respective groups of
rats. After 1 hour inflammation is induced by injecting 0.1 ml of carrageenan into the
sub planter region of left hind paw of all the four groups of rats without disturbing the
normal behaviour.
i) Initial paw volume was recorded
ii) Immediately just after the injection of Carrageenan, Intalammation was
recorded
Observation of Anti inflammatory activity
i) The rats were held in a good position where the normal Physiological
functions should not be affected.
ii) The hind paw of the rats should be in the protruding position.
iii) The hind paw should be immersed in a ‘Y’ Shape tube of plethymograph.
Anti Inflammatory effect of Devadaru 78
Results
iv) Carrageenan induced hind paw after immersing the mercury level of ‘Y’
shape tube suddenly raised.
v) The raised mercury level was measured in mm
vi) That is the inflammation = raised mercury from ‘Y’ shape tube in mm.
vii) For group I treated with 1% Normal saline after induction of carrageenan
the decreased inflammation was calculated.
viii) For Group II treated with standard drug Ibuprofen suspension after
induction of carrageenan reduction of inflammation was calculated.
ix) For Group III treated with trial drug Aqueous extract after induction of
carrageenan reduction of Inflammation was recorded.
x) For Group IV treated with trial drug Alcoholic extract after induction of
Carrageenan reduction of Inflammation was recorded.
Anti Inflammatory effect of Devadaru 79
Results
Master Chart
Group SN Mark Paw Volume Recovery
or death
½ hr 1st hr 2nd hr 3rd hr
1 Head 0.11 0.24 0.31 0.40 Recovered
2 Body 0.12 0.22 0.32 0.42 "
3 Tail 0.11 0.23 0.31 0.44 "
4 Rt ft lb 0.12 0.24 0.33 0.40 "
5 Rt hd lb 0.11 0.23 0.31 0.43 "
1 Control
6 Lt hd lb 0.13 0.24 0.33 0.44 "
1 Head 0.043 0.09 0.14 0.11 "
2 Body 0.042 0.07 0.13 0.10 "
3 Tail 0.041 0.06 0.16 0.10 "
4 Rt ft lb 0.042 0.08 0.14 0.12 "
5 Rt hd lb 0.040 0.08 0.15 0.12 "
2
Standard
6 Lt hd lb 0.042 0.07 0.13 0.10 "
1 Head 0.10 0.21 0.28 0.38 "
2 Body 0.10 0.22 0.29 0.41 "
3 Tail 0.09 0.21 0.28 0.38 "
4 Rt ft lb 0.10 0.21 0.29 0.38 "
5 Rt hd lb 0.11 0.22 0.31 0.39 "
3
Aqueous
extract
200
mg/kg
body wt 6 Lt hd lb 0.10 0.20 0.30 0.39 "
1 Head 0.09 0.12 0.18 0.14 "
2 Body 0.08 0.14 0.19 0.14 "
3 Tail 0.08 0.12 0.18 0.12 "
4 Rt ft lb 0.07 0.12 0.17 0.13 "
5 Rt hd lb 0.08 0.14 0.18 0.12 "
4
Alcoholic
extract
200
mg/kg
body wt 6 Lt hd lb 0.09 0.12 0.18 0.14 "
Anti Inflammatory effect of Devadaru 80
Results
Table No. 4.3 Parameter I - Showing the readings of paw volume of all the
groups of Rats after ½ hr
Samples Control group(Group I)
Standard group
(Group II)
Trial group A (Group III)
Trial group B (Group IV)
1 0.11 0.043 0.10 0.09 2 0.12 0.042 0.10 0.08 3 0.11 0.041 0.09 0.08 4 0.12 0.042 0.10 0.07 5 0.11 0.040 0.11 0.08 6 0.13 0.042 0.10 0.09
Table No. 4.4 Summary of Data
S.L.No
Group Samples Mean Standard deviation
Standard error of
mean
Median
1 Control 6 0.116 0.0081 0.0033 0.115 2 Standard 6 0.041 0.0010 0.00042 0.042 3 Trial group A
(Aq extract) 6 0.081 0.0075 0.0030 0.080
4 Trial group B (Alc extract)
6 0.100 0.0063 0.0025 0.100
Table No 4.5 Anova Table
S.L.No
Source of variation
Degree of
freedom
Sum of squares
Mean squares
F Value
1 Treatment 3 0.0187 0.0062 2 Residuals 20 0.00082 4.110 3 Total 23 0.01952 151.66
Table No. 4.6 Comparison
SL.no Comparison Mean difference
t value P value
1 Ct Vs std 0.0750 28.656 p < 0.001 2 Ct Vs Aq 0.016 6.36 p < 0.01 3 Ct Vs Alc 0.0350 13.37 p < 0.001 4 Std Vs Aq - 0.058 22.28 p < 0.001 5 Std Vs Alc - 0.040 15.28 p < 0.001 6 Aq Vs Alc - 0.018 7.005 p < 0.001
Anti Inflammatory effect of Devadaru 81
Results
Graph. 1
Paw volume observed in Individual Rat of control group
0.11 0.12 0.11 0.12 0.110.13
0
0.05
0.1
0.15
0.2
0.25
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 1/2 Hour
Graph. 2
Paw volume observed in Individual Rat of Standard group
0.043 0.042 0.041 0.042 0.04 0.042
0
0.05
0.1
0.15
0.2
0.25
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 1/2 Hour
Anti Inflammatory effect of Devadaru 82
Results
Graph. 3
Paw volume observed in Individual Rat of Trial group A (Aqueous extract)
0.1 0.1 0.09 0.1 0.11 0.1
0
0.05
0.1
0.15
0.2
0.25
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 1/2 Hour
Graph. 4
Paw volume observed in Individual Rat of Trial group B (Alcoholic extract)
0.09 0.08 0.08 0.07 0.08 0.09
0
0.05
0.1
0.15
0.2
0.25
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 1/2 Hour
Anti Inflammatory effect of Devadaru 83
Results
Table No. 4.7 Parameter II Showing the readings of paw volume of all the
groups of Rats after 1 hr
Samples Control group(Group I)
Standard group
(Group II)
Trial group A (Group III)
Trial group B (Group IV)
1 0.24 0.09 0.21 0.12 2 0.22 0.07 0.22 0.14 3 0.23 0.06 0.21 0.12 4 0.24 0.08 0.21 0.12 5 0.23 0.08 0.22 0.14 6 0.24 0.07 0.20 0.12
Table No. 4.8 Summary of Data
S.L.No
Group Samples Mean Standard deviation
Standard error of
mean
Median
1 Control 6 0.233 0.00816 0.0033 0.235 2 Standard 6 0.075 0.01049 0.0042 0.075 3 Trial group A
(Aq extract) 6 0.211 0.0075 0.0030 0.210
4 Trial group B (Alc extract)
6 0.126 0.0103 0.0042 0.120
Table No 4.9 Anova Table
S.L.No
Source of variation
Degree of
freedom
Sum of squares
Mean squares
F Value
1 Treatment 3 0.09823 0.03274 2 Residuals 20 0.001700 8.500 3 Total 23 0.09993 385.23
Table No. 4.10 Comparison
SL.no Comparison Mean difference
t value P value
1 Ct Vs std 0.158 42.06 p < 0.001 2 Ct Vs Aq 0.021 5.75 P < 0.01 3 Ct Vs Alc 0.106 28.34 p < 0.001 4 Std Vs Aq - 0.13 36.31 p < 0.001 5 Std Vs Alc - 0.051 13.72 p < 0.001 6 Aq Vs Alc - 0.085 22.58 p < 0.001
Anti Inflammatory effect of Devadaru 84
Results
Graph. 5
Paw volume observed in Individual Rat of Control group after 1 hour
0.24
0.22
0.230.24
0.230.24
0.2
0.25Pa
w V
olum
e
1 2 3 4 5 6Rat (Samples)
After 1 Hour
Graph. 6
Paw volume observed in Individual Rat of Standard group after 1 hour
0.090.07 0.06
0.08 0.08 0.07
0
0.05
0.1
0.15
0.2
0.25
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 1 Hour
Anti Inflammatory effect of Devadaru 85
Results
Graph. 7
Paw volume observed in Individual Rat of Trial group A (Aqueous extract) after
1 hour
0.21 0.22 0.21 0.21 0.220.2
0
0.05
0.1
0.15
0.2
0.25
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 1 Hour
Graph. 8
Paw volume observed in Individual Rat of Trial group B (Alcoholic extract) after
1 hour
0.120.14
0.12 0.120.14
0.12
0
0.05
0.1
0.15
0.2
0.25
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 1 Hour
Anti Inflammatory effect of Devadaru 86
Results
Table No. 4.11 Parameter III Showing the readings of paw volume of all the
groups of Rats after 2 hr
Samples Control group(Group I)
Standard group
(Group II)
Trial group A (Group III)
Trial group B (Group IV)
1 0.31 0.14 0.28 0.18 2 0.32 0.13 0.29 0.19 3 0.31 0.16 0.28 0.18 4 0.33 0.14 0.29 0.17 5 0.31 0.15 0.31 0.18 6 0.33 0.13 0.30 0.18
Table No. 4.12 Summary of Data
S.L.No
Group Samples Mean Standard deviation
Standard error of
mean
Median
1 Control 6 0.318 0.009 0.0040 0.315 2 Standard 6 0.141 0.011 0.0047 0.140 3 Trial group A
(Aq extract) 6 0.291 0.011 0.0047 0.290
4 Trial group B (Alc extract)
6 0.180 0.006 0.0025 0.180
Table No 4.13 Anova Table
S.L.No
Source of variation
Degree of
freedom
Sum of squares
Mean squares
F Value
1 Treatment 3 0.1312 0.0437 2 Residuals 20 0.00205 0.00010 3 Total 23 0.1333 426.28
Table No. 4.14 Comparison
SL.no Comparison Mean difference
t value P value
1 Ct Vs std 0.1767 42.06 p < 0.001 2 Ct Vs Aq 0.026 5.75 P < 0.01 3 Ct Vs Alc 0.138 28.34 p < 0.001 4 Std Vs Aq - 0.150 36.31 p < 0.001 5 Std Vs Alc - 0.038 13.72 p < 0.001 6 Aq Vs Alc - 0.111 22.58 p < 0.001
Anti Inflammatory effect of Devadaru 87
Results
Graph. 9
Paw volume observed in Individual Rat of Control group after 2 hour
0.31 0.32 0.31 0.33 0.31 0.33
00.05
0.10.15
0.20.25
0.30.35
0.4
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 2 Hour
Graph. 10
Paw volume observed in Individual Rat of Standard group after 2 hour
0.14 0.130.16
0.14 0.150.13
0
0.05
0.1
0.15
0.2
0.25
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 2 Hour
Anti Inflammatory effect of Devadaru 88
Results
Graph. 11
Paw volume observed in Individual Rat of Trial group A (Aqueous extract) after
2 hour
0.28 0.29 0.28 0.29 0.31 0.3
0
0.1
0.2
0.3
0.4
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 2 Hour
Graph. 12
Paw volume observed in Individual Rat of Trial group B (Alcoholic extract) after
2 hour
0.18 0.19 0.18 0.17 0.18 0.18
0
0.05
0.1
0.15
0.2
0.25
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 2 Hour
Anti Inflammatory effect of Devadaru 89
Results
Table No. 4.15 Parameter IV Showing the readings of paw volume of all the
groups of Rats after 3 hr
Samples Control group(Group I)
Standard group
(Group II)
Trial group A (Group III)
Trial group B (Group IV)
1 0.40 0.11 0.38 0.14 2 0.42 0.10 0.41 0.14 3 0.44 0.10 0.38 0.12 4 0.40 0.12 0.38 0.13 5 0.43 0.12 0.39 0.12 6 0.44 0.10 0.39 0.14
Table No. 4.16 Summary of Data
S.L.No
Group Samples Mean Standard deviation
Standard error of
mean
Median
1 Control 6 0.421 0.018 0.0074 0.425 2 Standard 6 0.108 0.0098 0.0040 0.405 3 Trial group A
(Aq extract) 6 0.388 0.011 0.0047 0.385
4 Trial group B (Alc extract)
6 0.131 0.0098 0.0040 0.135
Table No 4.17 Anova Table
S.L.No
Source of variation
Degree of freedom
Sum of squares
Mean squares
F Value
1 Treatment 3 0.492 0.164 2 Residuals 20 0.0033 0.00016 3 Total 23 0.4957 984.63
Table No. 4.18 Comparison
SL.no Comparison Mean difference
t value P value
1 Ct Vs std 0.313 59.45 p < 0.001 2 Ct Vs Aq 0.033 6.82 P < 0.01 3 Ct Vs Alc 0.290 55.02 p < 0.001 4 Std Vs Aq - 0.280 53.12 p < 0.001 5 Std Vs Alc - 0.023 4.42 p < 0.05 6 Aq Vs Alc - 0.25 48.69 p < 0.001
Anti Inflammatory effect of Devadaru 90
Results
Graph. 13
Paw volume observed in Individual Rat of Control group after 3 hour
0.4 0.42 0.440.4 0.43 0.44
0
0.1
0.2
0.3
0.4
0.5
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 3 Hour
Graph. 14
Paw volume observed in Individual Rat of Standard group after 3 hour
0.11 0.1 0.10.12 0.12
0.1
0
0.05
0.1
0.15
0.2
0.25
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 3 Hour
Anti Inflammatory effect of Devadaru 91
Results
Graph. 15
Paw volume observed in Individual Rat of Trial group A (Aqueous extract) after
3 hour
0.38 0.41 0.38 0.38 0.39 0.39
0
0.1
0.2
0.3
0.4
0.5
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 3 Hour
Graph. 16
Paw volume observed in Individual Rat of Trial group B (Alcoholic extract) after
3 hour
0.14 0.140.12 0.13 0.12
0.14
0
0.05
0.1
0.15
0.2
0.25
Paw
Vol
ume
1 2 3 4 5 6Rat (Samples)
After 3 Hour
Anti Inflammatory effect of Devadaru 92
Results
Table No. 4.19 Mean of all the groups for all the parameters
Group Treatment Mean ½ hr
Mean ±
SEM
Mean 1 hr
Mean ±
SEM
Mean 2 hr
Mean ±
SEM
Mean 3 hr
Mean ±
SEM
Recovery
or death
I Control
(Normal
saline)
0.116 ±
0.0033
0.233 ±
0.0033
0.318 ±
0.0040
0.421 ±
0.0074
Recovered
II Standard
(Ibuproten)
0.041 ±
0.0042
0.075 ±
0.0042
0.141 ±
0.0047
0.108 ±
0.0040
"
III Aqueous
extract
200mg/kg
0.081 ±
0.0030
0.211 ±
0.0030
0.291 ±
0.0047
0.388 ±
0.0047
"
IV Alcoholic
extract
200mg/kg
0.100 ±
0.0025
0.126 ±
0.0042
0.180 ±
0.0025
0.131 ±
0.0040
"
Graph. 17
Mean paw volume observed between the Groups
0.116
0.0410.081 0.1
0
0.1
0.2
0.3
Paw
vol
ume
Control Standard Trial Group A(Aq extract)
Trial Group B(Alc extract)
1/2 hour
Anti Inflammatory effect of Devadaru 93
Results
Graph. 18
Mean paw volume observed between the Groups
0.233
0.075
0.211
0.126
0
0.1
0.2
0.3P
aw v
olum
e
Control Standard Trial Group A(Aq extract)
Trial Group B(Alc extract)
1 hour
Graph. 19
Mean paw volume observed between the Groups
0.318
0.141
0.291
0.18
0
0.1
0.2
0.3
0.4
0.5
Paw
vol
ume
Control Standard Trial Group A(Aq extract)
Trial Group B(Alc Extract)
2 hour
Anti Inflammatory effect of Devadaru 94
Results
Graph. 20
Mean paw volume observed between the Groups
0.421
0.108
0.388
0.131
0
0.1
0.2
0.3
0.4
0.5
Paw
vol
ume
Contrlo Standard Trial Group A(Aq extract)
Trial Group B(Alc Extract)
3 Hours
Anti Inflammatory effect of Devadaru 95
Results
Statistical Analysis
The data obtained through the experimental study as shown in the tables bring
analyzed statistically based on the student t-test values as follows
• In the control group the result was non significant with p valuse > 0.10
• In standard group the result was highly significant with p value < 0.0001
• In the trial group (Alcoholic extract) the result was highly significant with p
value 0.001
• Comparison between group I (control) & Group II standard drug Ibuprofen
was highly significant that the control group (significant at 5%)
• Comparison between Group I & Group III. Aqueous extract of Devadaru (G
III) is better than the control group (G I) (Significant at 2%)
• Comparison between Group I & Group IV, Alcoholic extract was highly
significant than the control group.
• Comparison between group II & III standard drug is highly significant group
III is moderately significant.
• Comparison between II & IV both groups are highly significant.
• Comparison between III & IV Alcoholic extract ( G4) was highly significant
than group III.
Therefore by observing all the statistical results it can be ascertained that
Devadaru plays a highly significant role with Alcoholic extract and significant
role with Aqueous extract in reducing inflammation being equally effective as the
standard drug Ibuprofen.
Anti Inflammatory effect of Devadaru 96
Discussion
DISCUSSION
The title of the present study is “Preliminary phyto chemical investigation and
Anti-inflammatory effect of “Devadaru” on Albino rats” An experimental
study.
This Protocol includes the systemic study of the ideal drug Devadaru,
Phytochemical study for determination of different chemical components in
the trial drug experiment study is done for Anti-inflammatory activity.
In Ayurveda there are so many drugs mentioned under the Anti-inflammatory
property, among them Devadaru (cedrus- deodara) is one of the most potent
anti-inflammatory drug.
The present study is of Phytochemical and experimental study of Devadaru,
with its special reference to anti-inflammatory activity, under this the literature
review, disease review, aims and objects of Devadaru are studied. The
materials & methods observations and results were discussed and concluded.
Shotha, shopha and shwayathu the terms used may be different in different
contexts, but all our acharyas has given much importance to this condition.
They have devoted separate chapters for the description of the Nidana
panchakas and chikitsa,
Shushruta while describing the Nirukti of shopha, “Ekadeshothitha shopha
ityuchyate” meaning oedema arising in any one part of the body is shopha
while describing vishesha laxanas of shopha. He uses the word shwayathu,
which has also been used during description of sarva sara shopha, so it may be
under stood that all the three terms are synonymous.
To understand the disease entity for experiments based on modern science, an
attempt has been made by putting correlation between shotha & inflammation.
Anti Inflammatory effect of Devadaru 97
Discussion
This is according to the respective explainations of the similarities in their
symptoms.
Inflammation is local response of living mammalian tissues elicited as a
defence reaction in order toeliminate or limit the spread of injurious agents as
well as to remove the consequent necrosed cells & tissues.
A series of phenomenon including increase in the vascular permeability,
accumuolation of exudates and bringing into action of many mediators like the
prosta glandin etc. that play an important role are sent into action.
Till the date a number of studies have been carried out to screen the various
herbs, for anti-inflammatory action to put fourth the alternative diseases.
Herbal remedy which could take the place of the synthetic drug of the new era.
The drug Devadaru mainly grows in north-western himalayas, having the
properties like Tikta, katurasa, Laghu snigda guna, ushna veerya & katu
vipaka.
Stem bark of Devadaru is taken for the present study.
The drug was identified by botanists & faculty members of PG department of
Dravyaguna before beginning the study.
Discussion of Phytochemical analysis
Here the Phytochemical study performed to identify the active chemical
components such as alkaloids, sterols, carbohydrates, tri-terpinods & tannins
etc.
Both Aqueous & Alcoholic extracts of Devadaru were subjected for chemical
texts different chemical constituents such as alkaloids with yellow precipitates
carbohydrates with brick red precipitates, sterols with red precipitates,
Anti Inflammatory effect of Devadaru 98
Discussion
Triterpenoids with yellow precipitate, Tannins with white precipitate indicates
presence of active components.
Discussion on Identification by TLC method
By following the appropriate methodology of TLC preparation, black spot was
observed on TLC plate. This spot indicates the active chemical components present
inside the diluted solutions.
Discussion on experimental study
The design of the study on inflammation was made on animal experimentation
on Albino rats weighing between 150-200 gms were selected. Four groups
made based on the following pattern.
Group I – Control group 1% normal saline was fed orally to the albino rats at
the dosage of 0.2 ml/200gms body weight each animal in the single dose.
Group II – Standard group: Ibuprofin suspension was purchased and fed orally
to the albino rats at the dosage of 162 mg/kg. Body weight.
Group III – Trial group A – Aqueous extract was weighed and given to trial
group A to all the albino rats at the dosage of 200mg/kg body weight.
Group IV – Trial group B alcoholic extract was weighed and given to trial
group B to all the albino rats at the dosage of 200mg/kg body weight.
Carrageenan 0.1ml was used to induce inflammation in the left hind paw of
all the rats keeping the right paw as control. The paw volume of the rats of
four groups before and after injecting carrageenan inflammation was measured
using plethysmograph, paw volume was measured hourly for three hours after
injecting the carrageenan & observations done to see the paw inflammation.
Inflammation was observed between 15-30 mins after induction of
caurageenan, on the analysis of observations it was found that the albino rats
Anti Inflammatory effect of Devadaru 99
Discussion
in the control group did not show any improvement by 3 hours but the rats in
the trial group A with aqueous extract have shown good response after 3
hours. Where as trial group B with Alcoholic extract & standard drug group
showed improvement during second and third hour of injecting carrageenan.
Statistical analysis showed that the result in a trial group with alcoholic
extract is almost nearer to that of standard group.
Development of oedema induced by carrageenan is commonly correlated with
the exudative stage of inflammation, one of the important processes of
inflammatory pathology. In the beginning of carrageenan injection there is
sudden elevation of paw volume in relation with histamine mediators, After
one hour the inflammation is increased gradually and was elevated during the
later 3 hours.
This second phase could be due to the liberation of prosto glandin & kninins,
which accompanies leucocytes migration.
Animal experimentation has its limitation in the evaluation of inflammation,
all the symptoms cannot be evaluated as done in clinical study here only the
utseda can be evaluated through the aid of plethismography by which the
reduction of inflammation can be calculated.
All the statistical data and graphs were presented in the tables.
Thus through animal experimentation it was found that Devadaru has highly
significant action as anti-inflammatory drug with alcoholic extraction, where
as moderately significant action with Aqueous extract.
The samprapti of shotha begins by vitiation of kapha, Rakta and pitta which
enter the bahya siras and in turn vitiates the vata located there. Thus sroto
rodha is caused which spreads to the area in the viscinity & shotha results.
Anti Inflammatory effect of Devadaru 100
Discussion
The drug Devadaru is Tikta in rasa, laghu in guna, ushna veerya & katu
vipaka, ushna veerya is known to act on vata and kapha & tikta rasa reduces
pitta and cleans the rakta, laghu guna also acts antagonistically on kapha, katu
vipak in the drug contracts organic tissues and lessons its secretions and in
practice it is found that the katu effect, some times tend to overlap with anti-
inflammatory activity to some extent.
Thus the gunas of trial drug act all together upon pitta, rakta, kapha during
samprapti vighatana and eventually pacified these, once vitiated pitta, rakta
and kapha are brought to the normal state the vayu gets pecified thus clearing
the sroto rodha relieving shotha.
Anti Inflammatory effect of Devadaru 101
Conclusion
CONCLUSION
• Review of classical and Modern literaures shows that the trial drug Devadaru
is having significant shothahara property.
• Devadaru is having katu, Tikta rasa, Laghu snigda gunas Ushna veerya and
Katu vipaka.
• Devadaru [Cedrus deodara ] belongs to Coniferae family.
• The useful part stem barks were collected and confirmed.
• Aqueous and Alcoholic extracts were prepared from coarse powder of stem
bark of Devadaru.
• Preliminary phytochemical investigations of both extracts were carried out.
• As per the phytochemical investigations sterols,Triterpenoids, Lipids,
Carbohydrates, Alkaloids, Tannins, Resins, Starch, oils are present in both
extracts.
• Rats were selected randomly weighing between 150-200gm
• 0.1 ml of carrageenan was injected into the sub plantar region of left hind paw
to induce inflammation.
• Aqueous extract 200mg / kg and alcoholic extract 200mg / kg body weight
was given to third and fourth group respectively. Therapeuctic effect for
inflammation was observed in both the groups.
• Inflammation was measured through plethysmograph.
• Shotha manifests as disease it self and also as associated symptom.
• Comparing the results from the control, trial groups especially makes out
inhibition activities of Devadaru in inflammation.
• Aqueours extract of Devadaru (G III) is effective in inhibiting the
inflammation when compared with control group (GI)
Anti Inflammatory effect of Devadaru 102
Conclusion
• Alcholic extract of Devadaru (G IV) is more efficacious in comparison with
both Aqueous and control group (GI & GIII)
• Statistically trial drug Alcoholic extract & standard drug are equipotent.
• Summarizing the above it is concluded that alcoholic extract of Devadaru (G
IV) is highly significant when compared to aqueous extract (G III).
• It is obvious to document, the Alcoholic extract of Devadaru (G IV) has
showed its extreme utility or significance on the inflammation probably
because of its excellent activity of inhibiting prostaglandin synthesis which is
one of the cause for inflammation.
• As per documented experimental studies and analysis of classical literature it
is also noted the reason for the inhibition of inflammation is possible by the
aid of Tikta rasa & ushna veerya properties of the dravya.
Scope for future study
• The study was conducted with one paradigm i.e carageenan induced, other
paradigm like crotonoil induced granuloma pouch, cotton pellet implantation
method etc. can be tested.
• To assess the claim made on Devadaru in regarding inflammation clinical
study is necessary in all phases.
• To get scientifically based description of histo pathology of cells or tissues
Pharmacological study is necessary.
• Higher Phyto chemical investigations are required for the confirmatory
evaluation of responsible phyto constituents contributing to anti inflammatory
activity.
Anti Inflammatory effect of Devadaru 103
Summary
SUMMARY
The present dissertation entitled “Priliminary phytochemical investigation and
shothahara (Anti-inflammatory) effect of Devadaru (cedrus deodara) on Albino rats -
An experimental study” Comprises of 7 chapters can be summarized as follows
I) Objectives
II) Review of Literature
a) Drug review
b) Disease review
III) Methodology
IV) Results
V) Discussion
VI) Conclusion
VII) Summary
A part from all these in the part of introduction at the beginning, importance of
Dravya guna branch, significant of herbal plant, preparation necessity for the
assortment of this research work aims and objectives materials and methods and plan
of present study is mentioned.
First chapter objectives at the beginning gives an idea of aims & objectives of
present study and design of present research work.
Second chapter Review of literature consists of literature review of drug
Devadaru & literately review of disease shotha drug review induces both ayurvedic as
well as modern aspect. In Ayurvedic aspect History, synonyms, Guna, Varga, Bheda,
Guna, Karma, Prayojynaga, Matra, Prayoga, vishita yoga etc. all these matter
described.
Anti Inflammatory effect of Devadaru 104
Summary
In modern drug review classification (division, subdivision, class, subclass,
order family, genus, species) distribution, phytochemestry, therapeutic uses all these
thing are described in detail.
The majority of reference described Devadaru has katu, Tikta rasa Laghu
snigda guna, Ushnaveerya and katu vipaka acts as Deepaka, pachan, Vrana shodhaka,
vranaroopana, shothahara etc because of these reasons one can conceptualize that
drug must be effective in the treatment of shotha & other condition related with it.
Disease review includes both Ayurvedic as well as modern aspect. In
Ayurvedic literature as well as modern aspect. In Ayurvedic literature inflammation
has been described under various terms like shotha, shopha, shwayathu, but all these
terms used in similar meaning because of this reason shotha has more nearer meaning
to the kind of inflammation.
Methodology is the 3rd chapter deals with materials and methods which were
used in present work.
Observations statistical data, statistical analysis & reserves and explained in
4th chapter ie results fifth chapter is the discursion part here discussion of preliminary
phytochemical investigation of Devadaru, TLC experimentation & about results was
done over the experimental & statistical study.
Sixth chapter is by observing and analyzing the results obtained during this
study a conclusion was drawn finally the essence of this dissertation has been
explained in 7th chapter i.e., summary.
Anti Inflammatory effect of Devadaru 105
Bibilography
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73) Agnivesha, Charaka samhita, Vol-2, Chikitsa sthana, Chapter 12, Shloka
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Anti Inflammatory effect of Devadaru 112
Bibilography
74) Sushruta, Sushruta samhita, Vol-1st, Chikitsa sthana, Chapter 23, Shloka 12.
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P.103.
75) Vagbhata, Astangahridayam, Vol-2, Chikitsasthana, Chapter 17, Shloka 1-2.
K.R Shrikantamurthy editor. Varanasi: Krishnadasa academy; 1995. P.269.
76) Agnivesha, Charaka samhita, Vol-2, Chikitsa sthana, Chapter 12, Shloka
25,53 & 54. Brahmananda tripati Varanasi: Choukambha surabharati
prakashan: 2001. Pg. 438.
77) Vagbhata, Astangahridayam, Vol-2, Chikitsasthana, Chapter 17, Shloka 1-2.
K.R Shrikantamurthy editor. Varanasi: Krishnadasa academy; 1995. P.269.
78) Sudarshana shastri, Madhava Nidana Vol-II, Varanasi, Chaukamba orientalia;
Pg. 46.
79) Agnivesha, Charaka samhita, Vol-2, Chikitsa sthana, Chapter 12, Shloka
25,53 & 54. Brahmananda tripati Varanasi: Choukambha surabharati
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80) Sushruta, Sushruta samhita, Vol-1st, Chikitsa sthana, Chapter 23, Shloka 12.
Kavirajaambikadattashastri ed. Varanasi: Choukambha sanskrita sansthana;
P.103.
81) Vagbhata, Astangahridayam, Vol-2, Chikitsasthana, Chapter 17, Shloka 1-2.
K.R Shrikantamurthy editor. Varanasi: Krishnadasa academy; 1995. P.268.
82) Sudarshana shastri, Madhava Nidana Vol-II, Varanasi, Chaukamba orientalia;
Pg. 46.
83) Agnivesha, Charaka samhita, Vol-2, Chikitsa sthana, Chapter 12, Shloka
25,53 & 54. Brahmananda tripati Varanasi: Choukambha surabharati
prakashan: 2001. Pg. 439.
Anti Inflammatory effect of Devadaru 113
Bibilography
84) Vagbhata, Astangahridayam, Vol-2, Chikitsasthana, Chapter 17, Shloka 1-2.
K.R Shrikantamurthy editor. Varanasi: Krishnadasa academy; 1995. P.268.
85) Agnivesha, Charaka samhita, Vol-2, Chikitsa sthana, Chapter 12, Shloka
25,53 & 54. Brahmananda tripati Varanasi: Choukambha surabharati
prakashan: 2001. Pg. 439.
86) Agnivesha, Charaka samhita, Vol-2, Chikitsa sthana, Chapter 12, Shloka
25,53 & 54. Brahmananda tripati Varanasi: Choukambha surabharati
prakashan: 2001. Pg. 440.
87) Sushruta, Sushruta samhita, Vol-1st, Chikitsa sthana, Chapter 23, Shloka 12.
Kavirajaambikadattashastri ed. Varanasi: Choukambha sanskrita sansthana;
P.103.
88) Vagbhata, Astangahridayam, Vol-2, Chikitsasthana, Chapter 17, Shloka 1-2.
K.R Shrikantamurthy editor. Varanasi: Krishnadasa academy; 1995. P.268.
89) Agnivesha, Charaka samhita, Vol-2, Chikitsa sthana, Chapter 12, Shloka
25,53 & 54. Brahmananda tripati Varanasi: Choukambha surabharati
prakashan: 2001. Pg. 440.
90) Sushruta, Sushruta samhita, Vol-1st, Chikitsa sthana, Chapter 23, Shloka 12.
Kavirajaambikadattashastri ed. Varanasi: Choukambha sanskrita sansthana;
P.103.
91) Vagbhata, Astangahridayam, Vol-2, Chikitsasthana, Chapter 17, Shloka 1-2.
K.R Shrikantamurthy editor. Varanasi: Krishnadasa academy; 1995. P.268.
92) Agnivesha, Charaka samhita, Vol-2, Chikitsa sthana, Chapter 12, Shloka
25,53 & 54. Brahmananda tripati Varanasi: Choukambha surabharati
prakashan: 2001. Pg. 440.
Anti Inflammatory effect of Devadaru 114
Bibilography
93) Sushruta, Sushruta samhita, Vol-1st, Chikitsa sthana, Chapter 23, Shloka 12.
Kavirajaambikadattashastri ed. Varanasi: Choukambha sanskrita sansthana;
P.103.
94) Vagbhata, Astangahridayam, Vol-2, Chikitsasthana, Chapter 17, Shloka 1-2.
K.R Shrikantamurthy editor. Varanasi: Krishnadasa academy; 1995. P.269.
95) Ibid
96) Agnivesha, Charaka samhita, Vol-2, Chikitsa sthana, Chapter 12, Shloka
25,53 & 54. Brahmananda tripati Varanasi: Choukambha surabharati
prakashan: 2001. Pg. 440.
97) Sushruta, Sushruta samhita, Vol-1st, Chikitsa sthana, Chapter 23, Shloka 12.
Kavirajaambikadattashastri ed. Varanasi: Choukambha sanskrita sansthana;
P.103.
98) Ibid
99) Ibid
100) Vagbhata, Astangahridayam, Vol-2, Chikitsasthana, Chapter 17, Shloka 1-2.
K.R Shrikantamurthy editor. Varanasi: Krishnadasa academy; 1995. P.269.
101) Ibid
102) Agnivesha, Charaka samhita, Vol-2, Chikitsa sthana, Chapter 12, Shloka
25,53 & 54. Brahmananda tripati Varanasi: Choukambha surabharati prakashan:
2001. Pg. 441.
103) Ibid
104) Ibid
Anti Inflammatory effect of Devadaru 115
Bibilography
105) Agnivesha, Charaka samhita, Vol-2, Chikitsa sthana, Chapter 12, Shloka
25,53 & 54. Brahmananda tripati Varanasi: Choukambha surabharati prakashan:
2001. Pg. 454 & 442.
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Anti Inflammatory effect of Devadaru 116
Annexure
ANNEXURE Table 3.1 Protocol of experimental study:
Group Sl.No Dose Paw Volume Recovery or death
½ hr 1st hr 2nd hr 3rd hr 1 2 3 4 5
1 Control
6 1 2 3 4 5
2
Standard (Ibuprofen)
6 1 2 3 4 5
3 Trial Group A Aqueous
extract 200 mg/kg
body wt 6 1 2 3 4 5
4 Trial Group B Alcholic
extract 200 mg/kg
body wt 6
Anti Inflammatory effect of Devadaru 117
Slokas
Slokas of Devadaru
• SåuÉÉSÉ xqÉ×iÉÇ SÉÂpÉSìÇ SÉÌuÉïuSìSÉ cÉ | qÉxiÉSÉ SìÓÌMüÍsÉqÉÇ ÌMüÍsÉqÉÇ xÉÑUpÉÔÂWûÈ || 24 || (pÉÉ.mÉë.ÌlÉ)
• SåuÉÉSÉ sÉkÉÑ ÎxlÉakÉÇ ÌlÉ£üÉåwhÉÇ MüOÒûmÉÉÌMü cÉ | ÌuÉoÉlkÉÉkqÉÉlÉzÉÉåjÉÉqÉiÉuSìÉÌWû‚ÉeuÉUÉx§ÉÉÎeÉiÉç | mÉëqÉåWûmÉÏlÉxÉzsÉåwqÉMüÉxÉMühQÕûxÉqÉÏUlÉÑiÉ || 25|| (pÉÉ.mÉë.ÌlÉ)
• SåuÉSÉ UxÉå ÌiÉ£Çü ÎxlÉakÉÉåwhÉÇ zsÉåwqÉuÉÉiÉÉÎeÉiÉç |
AÉqÉSÉåwÉÌuÉoÉlkÉÉÅÅkqÉmÉëqÉåWûÌuÉÌlÉuɨÉïMüqÉë || SåuÉSÉuÉïÌlÉsÉÇ WûÎliÉ ÎxlÉakÉÉåwhÉÇ zsÉåwqÉmÉÉMüiÉÈ || (kÉ.ÌlÉ)
• SåuÉSÉ xqÉ×iÉÇ SÉ xÉÑUÉÀÇûû ÌMüÍsÉqÉÇ cÉ iÉiÉç |
xlÉåWûÌuÉ¬Ç qÉWûÉSÉ pÉSìSÉÌuÉïlSì SÉ cÉ ||75|| (kÉ.ÌlÉ)
• SåuÉMüÉ¸Ç pÉSìMüÉ¹Ç mÉÔÌiÉMüÉ¸Ç xÉÑSÉ cÉ | xÉÑUSÉÌuÉïlSìuÉ×¤É¶É iÉjÉæuÉÉqÉUSÉ cÉ || 76 || (kÉ.ÌlÉ)
• SåuÉSÉ UxÉå ÌiÉ£Çü ÎxlÉakÉÉåwhÉÇ zsÉåwqÉuÉÉiÉÉÎeÉiÉç | AÉqÉSÉåwÉÌuÉoÉlkÉÉkqÉ mÉëqÉåWûÌuÉÌlÉuɨÉïMüqÉç || 77|| ((kÉ.ÌlÉ)
• SåuÉSÉÂ xÉÑUSÉÂ SÉÂMÇü ÎxlÉakÉSÉÂUqÉUÉÌSSÂ cÉ |
pÉSìSÉÂ, ÍzÉuÉSÉÂ zÉÉqpÉuÉÇ pÉÔiÉWûÉËU pÉuÉSÉÂ ÂSìuÉiÉç ||28|| (UÉ.ÌlÉ)
• ÎxlÉakÉSÉ xqÉ×iÉÇ ÌiÉ£Çü ÎxlÉakÉÉåwhÉÇ zsÉåwqÉuÉÉiÉÎeÉiÉç | AÉqÉSÉåwÉÌuÉoÉlkÉÉzÉïÈ – mÉëqÉåWûeuÉUÉlÉÉzÉlÉqÉç || 21|| (UÉ.ÌlÉ)
• SåuÉMüÉ¸Ç pÉSìMüÉ¸Ç SåuÉSÉ xÉÑUSÒqÉÈ |
zÉMüSìÓÈ ÌMüÍsÉqÉÇ SÉ pÉSìSÉ xÉÑUÉÀûûrÉÈ || 1309|| (Mæü.ÌlÉ)
• SåuÉMüÉ¸Ç sÉkÉÑ ÎxlÉakÉÇ ÌiÉ£üÉåwhÉÇ MüOÒûMÇü UxÉå | ÌuÉmÉÉMåü WûÉÎliÉ MüÉxÉÉqÉxuÉÉxÉÌWûkqÉÉMüTüÉÌlÉsÉlÉç || (1310) euÉUqÉåWûÌuÉoÉlkÉÉkqÉÉMühQÕûzÉÉåMüÉx§ÉmÉÏlÉxÉÉlÉç | (Mæü.ÌlÉ)
• SåuÉSÉÂ xÉÑUÉÀÇû xrÉÉ°SìSÉÂ xÉÑUSìÓqÉÈ |
pÉSìMüÉ¸Ç xlÉåWûuÉפÉÈ M×üÍqÉsÉÇ zÉ¢üSÉ cÉ || 92 || (qÉ.ÌlÉ)
• SåuÉÉSÉ MüOÒû ÎxlÉakÉÇ ÌiÉ£üÉåwhÉÇ sÉkÉÑ lÉÉzÉrÉåiÉç | AÉkqÉlÉeuÉUzÉÉåjÉÉqÉÌWû‚ÉMühQÒûMüTüÉÌlÉsÉÉlÉç || 93|| (qÉ.ÌlÉ)
Anti Inflammatory effect of Devadaru
Slokas
EmÉrÉÉåaÉ – 1) cÉUMü – ÌWûMüÉμÉÉxÉrÉÉåÈ – _____ YuÉÉjÉqÉjÉuÉÉ SåuÉSÉÂhÉÈ || (cÉ. ÍcÉ 21/102) 2) xÉÑ´ÉÑiÉ – euÉUå ___ SåuÉSÉÂÍhÉ |
MüwÉÉrÉÇ ÌuÉkÉÏuÉiÉç MÔüiuÉÉ mÉårÉqÉåiÉeeuÉUÉmÉWûqÉç || E.39|| 3) zÉÉåjÉå _____ SåuÉSÉÂzÉÑhPûÏ uÉÉ qÉÔ§ÉåhÉ || (cÉ.ÍcÉ 23) uÉÉapÉOû 4) MüTüeÉMüÉxÉå MüTüMüÉxÉÉæ ÌmÉoÉåSÉSÉåï xÉÑUMüɸÉiÉç mÉëSÏÌmÉiÉÉiÉç |
xlÉåWÇû mÉËU´ÉÑiÉÇ urÉÉåwÉ rÉuɤÉÉUÉuÉ cÉÔÍhÉïiÉqÉç || (A.WØû.ÍcÉ. 3) WûÉUÏiÉ – 5) uÉÉiÉuÉëhÉå xÉÑUSÉ iÉjÉÉzÉÑhPûÏ sÉåmÉÉå uÉÉiÉuÉëhÉå ÌWûiÉÈ || (ÍcÉ. 35) cÉ¢üS¨É – 6) zsÉÏmÉSå – ÌWûiÉzrÉÉsÉåmÉlÉå ÌlÉirÉÇ ÍcɧÉMüÉå SåuÉSÉ uÉÉ | ------- xÉÑZÉÉåwhÉÉå qÉÔ§ÉmÉåÌwÉiÉÈ || (zÉsÉÏmÉSÍcÉÌMüixÉÉ) pÉÉuÉmÉëMüÉzÉ – 7) ¾ûSìaÉiÉåuÉÉiÉå SåuÉSÉÂxÉqÉÉrÉÑ£Çü lÉÉaÉUÇ mÉËUmÉÉåÌwÉiÉqÉç | ¾û²ÉiÉuÉåSlÉrÉÑ£üÈ mÉÏiuÉÉ xÉÑZÉqÉuÉÉmlÉÑrÉÉiÉç || (uÉÉiÉurÉÉÍkÉÍcÉÌMüixÉÉ) uÉÇaÉxÉålÉ 8) MüTüeÉaÉhQûqÉÉsÉÉrÉÉqÉ SåuÉSÉ ÌuÉzÉÉsÉÉ cÉ MüTüaÉhQåûmÉësÉåmÉlÉqÉç | (aÉsÉaÉhQûÍcÉÌMüixÉÉ) ÎzsÉmÉSå – 9) _____ SåuÉSÉ cÉ | ÌmÉoÉåixÉwÉïmÉiÉæsÉålÉ ÎzsÉmÉSÉlÉÉÇ ÌlÉuÉרÉrÉå || (ÎzsÉmÉSÉÍcÉÌMüixÉÉ ) 10) zÉÉåRûsÉ – MÑü¸å rÉLwÉ ¾Òû¹È ZÉÌSUxrÉ MüsmÉÈ xÉuÉÉïqÉrÉÉrÉÉÇ zÉqÉlÉå xÉqÉjÉïÈ| xÉLuÉ ÌlÉqoÉÉxÉlÉSåuÉSÉÂUÉåWûÏiÉMüÉUauÉkÉÍzÉÇzÉmÉÉlÉÉqÉç ||
Anti Inflammatory effect of Devadaru
Slokas
11) MühÉïzÉÔsÉå iÉæsÉÉ£üuÉx§ÉzÉMüsÉÉuÉ×iÉSåuÉSÉ – MüɸÉ̲ÌlÉÈxÉUÌiÉ rÉåeeuÉsÉlÉmÉëiÉmiÉÉiÉç | iɨÉæsÉqÉÉzÉÑ WûUÉÌiÉ ´ÉÑÌiÉUlkÉëmÉÏQûÉqÉç || 12) 11, ÌmÉssÉå pÉÉÌuÉiÉÇ oÉxiÉqÉÔ§ÉåhÉÇ xÉxlÉåWÇû SåuÉSÉ cÉ | ----------- ÌmÉssÉlÉÉzÉlÉqÉç || 13) UxɾÒûSrÉiÉl§ÉqÉç – mÉÌlÉxÉÉSÉæ xÉÑUiÉÂiÉæsÉÇ xÉbÉ×iÉÇ mÉÏiuÉÉ zÉÉsrÉÉåSlÉÇ cÉ xɤÉÏUqÉç | eÉÏhÉÉïWûÉUå pÉÑxiuÉÉ WûËUÌiÉ ÌWû MÑü¸ÉlÉç mÉÏlÉxÉÉSÏï¶É || (21-23)
Anti Inflammatory effect of Devadaru