Comparative Evaluation of Different Doses of Green Tea Extract Alone and in Combination with Sulfasalazine in Experimentally Induced Inflammatory Bowel Disease in Rats
- 200 Downloads
The exact etiopathology of inflammatory bowel disease is still unclear. Most of the therapies present are directed towards symptomatic improvement. Surgical therapy in the form of restorative proctocolectomy is reserved for the terminal stage disease, which is unresponsive to medical therapy. The present study was conducted to evaluate the effect of green tea in experimentally induced inflammatory bowel disease.
A total of 36 animals were included in the study. The animals were divided into five groups (n = 6): Group I-Vehicle (ethanol), group II-TNBS + ethanol, group III-green tea-treated group was divided into two sub-groups on the basis of different doses: group IIIA-TNBS + green tea (35 mg/kg), group IIIB-TNBS + green tea (70 mg/kg), group IV-TNBS + sulfasalazine (360 mg/kg), group V-TNBS + sulfasalazine (360 mg/kg) + green tea (least effective dose found in group III). After completion of 2 weeks of treatment, the rats were killed under ether anesthesia by cervical dislocation for assessment of intestinal inflammation, histological analysis, myeloperoxidase assay, malondialdehyde assay, and TNF-α estimation.
The study showed that green tea alone and in combination with sulfasalazine reduced inflammatory changes induced by tri nitro benzene sulfonic acid in rats. This reduction is associated with reduced malondialdehyde, lipid peroxidation, and TNF-α. This correlates well with both gross morphological and histopathological scores.
The authors concluded that a combination of green tea extract with sulfasalazine showed greater efficacy than single drug treatment.
KeywordsCrohn’s disease Ulcerative colitis Tumor necrosis factor Myeloperoxidase Malondialdehyde Interleukin-1
Analysis of variance
Complementary and alternative medicine
Committee for the Purpose of Control and Supervision on Experiments on Animals
Enzyme-linked immunosorbent assay
Institutional Animal Ethics Committee
Inflammatory bowel disease
Nuclear factor kappa-light-chain-enhancer of activated B cells
- PPAR γ
Peroxisome proliferator activated receptor γ
Retinoid X receptor
Tumor necrosis factor-α
Tri nitro benzene sulfonic acid
The authors have no financial or proprietary interests in any of the products mentioned in this manuscript. This study was funded by the Indian Council of Medical Research, Ansari Nagar, New Delhi.
- 1.Friedman S, Blumberg S. Inflammatory Bowel Disease. In: Kasper DL, Braunwald U, Fauci AS, Hauser SL, Longo DL, Jameson JL, eds. Harrison′s principles of internal medicine. 16th ed. New York: McGraw-Hill; 2005:1776–1788.Google Scholar
- 2.Kenneth M, Mc Quid MD. Alimentary tract. In: Lawrence MT, Stephen J, Macphee, Maxine A, Papadakis, eds. Current medical diagnosis and treatment. 42nd ed. Chicago: McGraw Hill; 2003:602–611.Google Scholar
- 3.Palmer KR, Penman ID. Disease of the alimentary tracts and pancrease. In: Haslett C, Chilvers ER, Hunter JAA, Boon NA, eds. Davidson’s principle and practice of medicine. 18th ed. United Kingdom: Churchill Livingstone; 1999:659–668.Google Scholar
- 14.Krawiesz JE, Sharan P, Stenson WF. Quantitative assay to acute intestinal inflammation based on myeloperoxidase activity: assessment of inflammation in rat and hamster model. Gastroenterol. 1984;87:1344–1350.Google Scholar
- 15.Ohkawa H, Ohishi N, Yoge K. Assay of lipid peroxides in animal tissue by thiobarbituric acid reaction. Anal Bio Chem. 1978;95:351–358.Google Scholar
- 16.Morris GP, Rebeiro L, Herride MM, Szewczuk M, Depew W. An animal model of chronic granulomatous inflammation of stomach and colon. Gastroenterol. 1985;86:1188.Google Scholar
- 17.Wallace JL, Hgaboam CM, Mc knight GW. PAF mediates gastric damage induced by hemorrhagic shock. Am J Physiol. 1990;259:140–146.Google Scholar