Download RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES KARNATAKA

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES
KARNATAKA, BANGALORE
M. PHARM SYNOPSIS
YEAR OF ADMISSION-SEPTEMBER 2010
TITLE OF THE SYNOPSIS
“Nephro-protective activities of Psidium guajava Linn. leaves extract in animal
models”
BY
Ms. NAIRUTI MANUBHAI PATEL M.PHARM
DEPARTMENT OF PHARMACOLOGY
UNDER THE GUIDANCE OF
Dr. BM. Vrushabendra Swamy, M.Pharm, Ph.D, FICCP
Director / Professor & Head
Department of Pharmacology
INSTITUTION
GAUTHAM COLLEGE OF PHARMACY
SULTHANPALYA, R.T. NAGAR, BANGALORE-560032
KARNATAKA
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,
BANGALORE, KARNATAKA
ANNEXURE-II
PROFORMA FOR REGISTRATION OF SUBJECT FOR DISSERTATION
1.
Name of The Candidate and
Address
Ms. NAIRUTI MANUBHAI PATEL
a. Permanent Address
D/o MANUBHAI K. PATEL,
22/4, Amardeep society,
Vijalpur road,
Navsari-396445,
Gujarat.
b.Postal Address
Gautham college of pharmacy,
Sulthan Palya, R.T. Nagar Post,
Bangalore-560032,
Karnataka.
2.
Name of The Institution
GAUTHAM COLLEGE OF PHARMACY
Sulthan palya, R.T Nagar.
Bangalore- 560032
3. Course of study and Subject
Master of Pharmacy in Pharmacology
4. Date of admission
07/09/2010
5. Title of the topic:
“Nephro-protective activities of Psidium guajava Linn. leaves extract in animal models”
6.0 BRIEF REVIEW OF THE INTENDED WORK:
6.1 INTRODUCTION:
The term renal failure primarily denotes failure of the excretory function of kidney,
leading to retention of nitrogenous waste products of metabolism in the blood. In addition,
there is failure of regulation of fluid and electrolyte balance along with endocrine dysfunction.
The renal failure is fundamentally categorized into acute and chronic renal failure1,2.
Chronic renal failure (CRF) is an irreversible deterioration in the renal function which
classically develops over a period of years, leading to loss of excretory metabolic and
endocrine functions. Various causes of renal failure has been attributed like hypertension,
diabetes mellitus, antineoplastic agents like cyclophosphamide, vincristin, cisplatin etc.
Acute renal failure (ARF) refers to the sudden and usually reversible loss of renal
function which develops over a period of days or weeks. There are many causes of acute
renal failure which could be pre-renal (55%), renal (40%), or post renal (5%). Among the
renal causes of acute renal failure, acute tubular necrosis is more common accounting for 85%
of incidence. Acute tubular necrosis occurs either due to ischemia or toxins. The toxin can
be either exogenous or endogenous.
The exogenous agents are radio contrast agents,
cyclosporin, antibiotics, chemotherapeutic agents, organic solvents, acetaminophen and illegal
abortifacients1,3.
Gentamicin is an important aminoglycoside antibiotic commonly used in treating life
threatening gram-negative infections4. However its usefulness is limited by signs of
nephrotoxicity, which may occur in 13-30% of treated patients5. Lipid peroxidation may
occur in the course of gentamicin administration6, giving rise to free radicals7, which are
highly toxic to tissue8. Oxidation and necrosis by apoptosis may occur.
Several distinct mechanisms have been proposed for cisplatin cytotoxicity in renal
tubule cells, including direct DNA damage9, activation of caspase10, mitochondrial
dysfunction11, formation of reactive oxygen species, 12 effects on the endoplasmic reticulum
13
and activation of TNF-α mediated apoptotic pathways. It has also been reported that
cisplatin induced nephrotoxicity is closely associated with an increase in lipid peroxidation in
the kidney. In addition, cisplatin has been found to lower the activities of Antioxidant
enzymes and to induce depletion of GSH.
Paracetamol also known as acetaminophen is widely used as analgesic and
antipyretic drug. An acute paracetamol overdosage can lead to potentially liver and kidney
failure in humans and experimental animals and in severe cases to death due to renal failure14,
15
. Paracetamol is a phenacetin metabolite16. Phenacetin was considered one of the most
nephrotoxic analgesics and has now been withdrawn from the market in many countries17.
A chronic nephrotoxic effect of therapeutic dosing of paracetamol is suggested by
case control studies.
Paracetamol induces acute renal damage by elevating plasma creatinine levels and
depleting glutathion levels. Tubular necrosis is observed histologically15. The fact that pamino phenol is formed from paracetamol in the kidney by deacetylation and its excretion in
urine, makes it a candidate for its role in the pathogenesis of paracetamol induced renal
damage18. The deacetylation contributes to paracetamol induced nephrotoxicity19. Also
hepatically derived glutathione conjugates are involved in paracetamol induced renal injury20.
Nitric oxide plays an important role in paracetamol induced renal damage in rat 21. Oxidative
stress plays a role in paracetamol induced liver damage and this contributes to the
pathogenesis of paracetamol induced renal damage.
Several plant products are known to exhibit credible medicinal properties for the
treatment of kidney ailments and need to be explored to identify their potential application in
prevention and therapy of human ailments.
6.2 NEED FOR THE STUDY:
Natural products are playing a vital role in health care for decades. Often different
sources of natural products, plants have been a source of chemical substance, which serves as
drugs in their own right or key ingredients in formulation containing synthetic drugs. The
selection of the plant species is a crucial factor for the ultimate success of investigation.
Through random selection gives some hint, targeted collection based on chemotaxonomic
relationships and ethnomedical information derived from Tradition Medicine are more likely
to yield pharmacologically active compounds. Although the advances in modern medicines
are significant, there remains an ever increasing demand for herbal medicines. Effective and
potent herbal medicines require evaluation by standard scientific methods so as to be
validated for the treatment of diseases.
Drug induced Nephro-toxicity is major health problem that challenges not only
healthcare professionals but also the pharmaceutical industry and also drug regulatory
agencies. The inhibition of free radical generation can serve as facile model for evaluating the
activity of Nephro-protective agents.
6.3 REVIEW OF LITERATURE:
Botanical name: Psidium guajava Linn.
Vernacular names: Guava (English)
Guayaba (Spanish)
Guajaba dulce (Colombia)
Guayaba blanca (Peru)
Family: Myrtaceae.
Distribution: It is distributed throughout in Mexico south and South America also in
Florida and West Indies.
Plant description:
Psidium guajava L. is a large shrub or small, evergreen, tree generally 3-10m high,
many branches stems tortuous, bark. Light to reddish brown, thin smooth, continuously
flaking; root system generally superficial and extensive, frequently extending well beyond
the canopy, there are some deep roots but no distinct taproot. Leaves: opposite, simple,
stipules absent; petioles short, 3-10mm long; blade oblong to elliptic, 5-15cm long, 4-6cm
wide, apex obtuse to bluntly acuminate, base rounded to subcuneate, margins entire, veins
prominent, gland dotted. Fruit: an ovoid or pear shaped berry 4-12cm long weighing up to
500g; skin yellow when ripe. Mesocarp thick edible. Seeds: kidney shaped or flattened22.
Traditional uses23-26:
The fruit is laxative and the seeds are astringent. The leaves of guava tree in
decoction are recommended for gastroenteritis, uterine hemorrhage, and chronic diarrhoea,
swollen legs etc. the young leaves and shoots are used for dysentery, inflammation of
kidney and
diarrhoea.
The
active
flavanoid
compound-
quarcetin-3-O-alpha-l-
arabinopyranoside (guaijaverin)-extracted from the leaves has high potential antiplaque
activity by inhibiting the growth of streptococcus mutans. An infusion or decoction made
from the leaves and/ or bark has been used by tribes for diarrhoea and dysentery
throughout Amazon. Indians also employ it for sore throats, vomiting, stomach upsets and
for vertigo. Decoction of bark/ leaves or flower infusion is used topically for wound, ulcers
and skin sores. Flowers are also mashed and applied to painful eye conditions such as sun
strain, conjunctivitis, eye injury.
Chemical constituents:
The fruit contains saponin combined with oleanolic acid. Morin-3-O-α-Llyxpyranoside and flavanoids, guajaverin and quercetin. The leaves contain essential oil
with main components being
α-pinene, β-pinene, limonene,methanol,terpenyl acetate,
isopropyl alcohol, longicyclene, cryophyllene, β-bisabolene, caryophyllene oxide, βcopanene, farnesene, humulene, selinene, cardinene and curcumene. The leaves also
contain an essential oil rich in cineol, and four triterpenic acids as well as three flavanoids
quercetin, avicularin, 3-L-4- pyranoside27.
Reported activities28-32:
Anti-diarrhoea
Anti-cough and anti-microbial
Anti-diabetic
Hepatoprotective
Anti-oxidant
6.4 OBJECTIVES OF THE STUDY:
The objective of the proposed study is to investigate the nephro-protective activity of
Psidium guajava Linn. hydroalcoholic extracts by using rats. Toxicological studies (LD50)
by using mice. The whole study is divided into two phases.
Phase I:

Collection and authentification of plant material.

Preparation of Psidium guajava Linn. hydroalcoholic leaves extract (70%v/v) using
Soxhlet apparatus.

To investigate preliminary phytochemical constituents present in the extract.

Determination of LD50 value and dose selection for the Nephro-protective activity(i.e.,
selection of two appropriate doses from the LD50 value) those doses considered as low and
high doses respectively.
Phase II:
To evaluate the nephro-protective activity of Psidium guajava Linn. leaves extracts in
various experimental animals models like:
 Gentamicin induced nephrotoxicity in rats.
 Cisplatin induced nephrotoxicity in rats.
 Paracetamol induced nephrotoxicity in rats.
Parameters to be studied:

Body weight determination.

Urine analysis – Sodium, Potassium, Glucose, Creatinine estimation.

Blood analysis- Urea, creatinine.

Histopathological studies.

Estimation of GSH and lipid peroxidation.
7.0 MATERIALS AND METHODS:
7.1 SOURCE OF DATA:
The sources of data will based on laboratory experiments on animals and also the
data obtained from the literature.
1. Standard Books:
 Goodman and Gilmann’s: The Pharmacological basis of Therapeutics.
 H.Gerhard Vogel’s: Drug Discovery and Evaluation
 Katzung’s : Basic and clinical pharmacology
 Rang and Dale’s: Pharmacology
 Tortora: Human Anotomy and Physiology
 Guyton and Hall’s: A Text Book of Medical Physiology
 Wealth of India
 Materia medica
 Glossary of Indian medicinal plants
2. Internet source:
 Pubmed
 www.sciencedirect.com
 SCOPUS
 Helinet
 Ovid
 Open J-Gate
 DOAJ
 Chemical Abstracts
 CABI
 Wikipedia
 Google
 International Pharmaceutical Abstracts
3. Journal sources:
 Indian Journal of Pharmacology
 Journal of Pharmacology and experimental Therapeutics
 Journal of Ethanopharmacology
 Phytochemistry
 American Journal of Pharmacology and Toxicology
7.2 METHOD OF COLLECTION OF DATA:
Materials:
1. Identification and authentification of the plant by Botanist.
2. All the chemicals used in this project will be analytical grade.
7.3 EXTRACTION OF PLANT MATERIAL:
About 150 g of powdered shade dried leaves of Psidium guajava Linn. will be
extracted with 70% v/v of ethyl alcohol by continuous heat extraction in a soxhlet extractor
for 24 hours, extract will be concentrated to small volume under reduced pressure and
evaporated to dryness. Further studies extract will be dissolved in distilled waters33.
7.4 EXPERIMENTAL ANIMALS:
Albino Wistar rats of either sex weight about 200-225g will be used and Albino mice
(20-25g) will be used for toxicological studies (LD50).
7.5 PLANT MATERIAL:
Naturally available leaves of Psidium guajava Linn. will be collected, identified and
extracted with hydroalcoholic solution.
7.6: ACUTE ORAL TOXICITY STUDY:
For this purpose female albino mice (20-25g) will be used. Fixed dose method
(OECD guideline no. 420) of CPCSEA will be adopted34.
DOSE:
The dose of hydroalcoholic extract of Psidium guajava Linn. will be calculated as per the
acute toxicity studies35.
7.7 NEPHRO PROTECTIVE ACTIVITY:
Nephro-protective activity will be studied using three models viz. gentamicin,
cisplatin, paracetamol induced nephrotoxicity models in rats.
 Study of protective effect of hydroalcoholic extract of Psidium guajava Linn. in
Gentamicin induced nephrotoxicity in rats36.
Nephrotoxicity in rats is to be induced with the administration of gentamicin (80mg/kg
i.p) for 8 days. The extract will be administered orally 3 days before the admintration of
gentmicin and continued for another 8 days along with gentamicin. The rats will be selected
and randomized into 4 groups, each group consisting of 6 animals. The extracts will be
administered orally and gentamicin will be administered intraperitoneally.
Animal
group
Group –I
Group-II
Treatment
Control
Gentamicin
Route of
administration
No of
Animals
used
------
6
Gentamicin +HAPG
Body weight
determination,
Intraperitoneally
6
Urine analysis–
Sodium, Potassium,
Glucose, Creatinine
estimation.
determination.
Intraperitonially
6
Blood analysis-Blood
urea nitrogen, serum
creatinine.
(80mg/kg)
Group-III
Parameters
80mg/kg+1/5thLD50
+ orally
Histophathological
study of kidney
Group-IV
Gentamicin +HAPG
Intraperitonially
80mg/kg+1/10thLD50
+ orally
HAPG-Hydro alcoholic extract of Psidium guajava Linn
6
Estimation of GSH
Lipid peroxidation
 Study of protective effects of hydroalcoholic extract of Psidium guajava Linn. in
paracetamol induced nephrotoxicity in rats37.
Nephrotoxicity in rats is to be induced with the administration of Paracetamol
(2g/kg oral) for 2 days. The extract (HAPG) will be administered orally 5 days before the
administration of paracetamol and continued for 7 days along with Paracetamol. Normal
control group will not be administered with either extract or paracetamol .The rats will be
selected and randomized into 4 groups each group consisting of 6 animals .The extract and
Paracetamol will be administered orally.
Animal
group
Treatment
Route of
administration
No of
Parameters
Animals
used
Body weight
Group –I
Control
------
6
determination.
Urine analysis–
Sodium, Potassium,
Group-II
Paracetamol (2g/kg)
Orally
6
Glucose, Creatinine
estimation. Blood
Group-III
Paracetamol
analysis-Blood urea
Orally + Orally
6
+HAPG
nitrogen, serum
2g/kg+1/5thLD50
creatinine
Histophathological study
of kidney.
Group-IV
Paracetamol+
Orally + Orally
HAPG
2g/kg+1/10thLD50
HAPG-Hydro alcoholic extract of Psidium guajava Linn.
6
Estimation of GSH
Lipid peroxidation
 Study of protective effects of hydroalcoholic, extract of Psidium guajava Linn. In
Cisplatin induced nephrotoxicity in rats38, 39.
Nephrotoxicity in rats is to be induced with the administration of cisplatin
(12mg/kg). The extract will be administered orally 1 hr before the administration of
cisplatin and at 24h and 48h after cisplatin injection. The parameters will be studied after
72h after cisplatin administration .The normal control group will not be administered
with either extract or cisplatin. The rats will be selected and randomized into 6 groups,
each group consisting of 6 animals.
Animal
group
Treatment
Route of
administration
No. of
Animals
used
Parameters
Control
------
6
Body weight
determination.
Group –I
(12mg/kg)
Urine analysis–
Sodium, Potassium,
Glucose, Creatinine
estimation.
Cisplatin +HAPG
Blood analysisBlood urea nitrogen,
serum creatinine.
Cisplatin
Group-II
th
Group-III
12mg/kg+1/5 LD50
Intraperitonially
Intraperitoneally
6
6
+
Histopathological
study of kidney
Orally
Group-IV
Cisplatin +HAPG
Intraperitoneally
12mg/kg+1/10thLD50
+
Orally
HAPG-Hydro alcoholic extract of Psidium guajava Linn.
6
Estimation of GSH
Lipid peroxidation
7.8 Statistical Analysis:
All the values that are generated out of this study execution will be expressed as
mean ± SEM from six animals. Statistical difference in mean will be analysed using one
way ANOVA (Analysis of Variance) followed by Dunnett’s‘t’ test. P values less than 0.05
were considered as indicative of significance40.
7.9 Does the study require any investigation or intervention to be conducted on patients
or other humans or animals? If so, please mention briefly.
Yes, the above study requires in vivo screening techiniques on wistar rats.
8. Has ethical clearance been obtained from your institution?
The copy of ethical clearance certificate is enclosed.
9. REFERENCES :
1. Herfindal, Gourley. Text book of therapeutic drug and disease management. 7th ed.
London: Charcil Livingstone; 2000. p. 425-36.
2. Barry M, Brenner, Floyd C, Rector. The kidney. 6th ed. Vol I, Philadelphia: W.B.
Saunders Company; 2000.p. 3-67.
3. Paul L Munson, Robert A Muller, George R Breese. Principles of pharmacology: Basic
concepts and clinical applications. Chapman and Hall ITP an International Thomson
publishing company: New York; 1996. p.685.
4. Ali BH. Gentamicin nephrotoxicity in humans and animals: Some recent research. Gen
Pharmacol 1995; 26(7): 1477-87.
5. Mathew TH. Drug-induced renal disease. Med J Aust 1992; 156: 724-28.
6. Ramsammy L, Ling KY, Josepovitz C, et.al. Effect of gentamicin on lipid peroxidation
in rat renal cortex. Biochem Pharmacol 1985; 34: 3895-900.
7. Yang C, Du X, Han Y. Renal cortical mitochondria are the source of oxygen free
radicals enhanced by gentamicin. Renal Fail 1995; 17: 21-26.
8. Feldman S, Wang M, Kaloyanides GJ. Aminoglycosides induce a phospholipidosis in
the renal cortex of the rat: An early manifestation of nephrotoxicity. J Pharmacol Exp
Therp 1982; 220: 514-20.
9. Leibbrandt ME, Wolfgang GH, Metz AL, Ozobia AA, Haskins JR. Critical subcellular
targets of cisplatin and related platinum analogs in rat renal proximal tubule cells.
Kidney Int 1995; 48:761-70.
10. Kaushal GP, Kaushal V, Hong X, Shah SV. Role and regulation of activation of
caspases in cisplatin induced injury to renal tubular epithelial cells. Kidney Int 2001;
60:1726-36.
11. Sugiyama S, Hayakawa M, Kato T, Hanaki Y, Shimizu K, Ozawa T. Adverse effects of
anti-tumor drug, cisplatin on rat kidney mitochondria: Disturbances in glutathione
peroxidase activity. Biochem Biophys Res Commun 1989; 159:1121-7.
12. Matsushima H, Yonemura K, Ohishi K, Hishida A. The role of oxygen free radicals in
cisplatin induced acute renal failure in rats. J Lab Clin Med 1998; 131:518-26.
13. Baliga R, Liu H. Activation of caspase 12 by cisplatin (CP) induced endoplasmic
reticulam (ER) stress mediates apoptosis in LLC-PK1 cells. Am Soc Nephrol 2004;
15:39.
14. Corina Lorz, Pilar Justo, Ana Sanz, Dolores Subira, Jesus Edigo, Alberto Ortiz.
Paracetamol induced renal tubular injury: A role for ER stress. J Am Soc Nephrol
2004; 15: 380-389.
15. Premila Abraham. Oxidative stress in paracetamol induced pathogenesis renal damage.
Indian J Biochem & Biophy 2005; 42: 59-62.
16. Prescott LF. Kinetics and metabolism of paracetamol and phenacetin. Br J Clin Pharm
1989; 10: 2915-2985.
17. De Broe ME, Elseviers MM. Analgesic nephropathy. N Engl J Med 1998; 338: 446452.
18. Carpenter HM, Mudge GH. Acetaminophen nephrotoxicity studies on renal acetylation
and deacetylation. J Pharm Exp Ther 1981; 218: 161-168.
19. Mugford CA, Tarlolf JB. Oxidative stress in paracetamol-induced pathogenesis: (I)
Renal damage. Toxicol Letter 1997; 93: 15-18.
20. Trumper L, Mansterolo LA, Elias MM. Nephrotoxicity of acetaminophen in male wistar
rats: role of hepatically derived metabolites. J Pharmacol Exp Ther 1996; 279:548-554.
21. Li C, Lui J, Saaedra JE, Keefer LK, Waalkes MP. The nitric oxide donor, VPYRRO/NO,
protects
against
acetaminophen-induced
nephrotoxicity in
mice.
Toxicology 2003; 189:173-180.
22. Food and fruit bearing forest species, 3: examples from latin America. 257.
23. Anthony C. Dweck FLS FRSC FRSH. A review of guava (Psidium guajava), Dweck
data.s
24. Ticzon, Romeo: Ticzon Herbal Medicine Encyclopedia. 1997. Romeo R. Ticzon
publishing Philippines. ISBN NO. 97191-7231-2.
25. Limsong J, Benjavong kulchai E, Kuvataanasuchati J. Inhibitory effects of some herbal
extracts on adherence of S. Mutans. J Ethnophrmacol 2004; 92(2-3): 281-289.
26. Tropical plant database, Raintree, Psidium guajava.www.raintree.com
27. Anthony C. Dweck FLS FRSC FRSH. A review of guava (Psidium guajava), Dweck
data.s
28. George D. Lutterodt. Inhibition of microlax-induced experimental diarrhoea with
narcotic-like extracts of Psidium guajava leaf in rats. J Ethnophrmacol 1992; 37(2): 151157.
29. Pranee Jaiarj, Paranee Khoohaswan, Yuwadee Wongkrajang, Penchom Peungvicha,
Potjanee Suriyawong, M. L. Sumal Saraya, Orawan Ruangsomboon. Anti-cough and
anti-microbial activities of Psidium guajava Linn. leaf extract. J Ethnophrmacol 1999;
67(2): 203-212.
30. Won keun oh et.al. Anti-diabetic effects of extracts from Psidium guajava Linn. J
Ethnophrmacol 2005; 96(3):411-415.
31. Chanchal K. Roy, Jagdish V Kamath and Mohammed Asad. Hepatoprotective activity of
Psidium guajava Linn leaf extract. Indian J Exp Biol 2006; 44: 305-311.
32. Soman S, Rauf AA, Indira M, Rajmanicka C. Anti-oxidant and anti-glycative potential
of ethyl acetate fraction of Psidium guajava Linn. leaf extract in streptozotocin-induced
diabetic rats. Plant Hum Nutr. 2010; 65(4): 386-391.
33. Madhavan V Yadav. DK, Murali A, Yoganarsimhan SN. Wound Healing Activity Of
Aqueous and Alcoholic Extracts Of Leaves of Clebrookea Oppositifolia Smith. Indian
Drugs 2009; 46(3).
34. Prema Veeraraghavan. Expert consultant, CPCSEA, OECD Guideline no.2000; 420.
35. Chanchal K. Roy, Jagdish V Kamath and Mohammed Asad. Hepatoprotective activity of
Psidium guajava Linn leaf extract. Indian J Exp Biol 2006; 44: 305-311.
36. Vijaj Kumar K, Naidu MUR, Anwar A, Shifow, Ratnakar KS. Probucol protects against
gentamicin induced nephrotoxicity in rats. Ind J Pharmacol 2000; 32: 108-13.
37. Milind A Khandkar, Dipak V Parmar, Mita Das, Surendra S Katyare. Is activation of
lysosomal
enzymes
responsible
for
paracetamol-induced
hepatotoxicity
and
nephrotoxicity?. J Pharm Pharmacol 1996; 48: 437-440.
38. Jisha Joy,Cherupally Krishnan Krishnan Nair. Amelioration of cisplatin induced
nephrotoxicity in Swiss albino mice by Rubia cordifolia extract. J Cancer Res Ther
2008; 4(3):111-115.
39. Corcostegui R, Labeaga L, Arteche JK, Orjales A. Protective effect of Hidrosmin against
cisplatin induced acute nephrotoxicity in rats. J Pharm Pharmacol 1998; 4: 465-467.
40. Chanchal K. Roy, Jagdish V Kamath and Mohammed Asad. Hepatoprotective activity of
Psidium guajava Linn leaf extract. Indian J Exp Biol 2006; 44: 305-311.
10.
SIGNATURE OF THE CANDIDATE:
11.
REMARK OF THE GUIDE
“Nephro-protective activity of Psidium guajava Linn. leaves extracts in animal
models.” to be carried out by Ms. NAIRUTI MANUBHAI PATEL of M. Pharm has
been discussed and worked out under my directions and supervision as an official
guide. The project work envisaged is of great importance in the field of pharmacology.
The work can be carried out in pharmacology laboratory of Gautham College of
Pharmacy for which facilities are available. Hence the project is viable and is
recommended for clearance and approval.
12.
NAME AND DESIGNATION OF:
12.1
GUIDE
Dr. BM. Vrushabendra Swamy
M.Pharm, Ph.D, FICCP
Director / Professor & Head
Department of Pharmacology
12.2
SIGNATURE
12.3
HEAD OF THE DEPARTMENT
Dr. BM. Vrushabendra Swamy
M.Pharm, Ph.D, FICCP.
Director / Professor & Head,
Department of Pharmacology.
12.4
13.
SIGNATURE
CLEARENCE FROM INSTITUTIONAL ETHICAL COMMITTEE:
The study is cleared from Animal Ethical Committee of the Institution.
(Approval no: 491/01/c/CPCSEA,) Enclosed Copy. Annexure-1
14.1
REMARK OF THE PRINCIPAL
The Program and the Research work that Ms. NAIRUTI MANUBHAI PATEL is
undertaking have potential implication in the field of Pharmacology. The work can be
carried out in the Research Laboratories of Pharmacology Department at Gautham
college of Pharmacy.
Hence the Project is recommended and requested for clearance and approval.
14.2
SIGNATURE
Prof. Archana Swamy. P M.Pharm (Ph.D)
Principal
Gautham College of Pharmacy
Bhuvaneswari nagar,
R.T.Nagar Post,
Bangalore- 32.