Digestive Diseases and Sciences

, Volume 56, Issue 5, pp 1369–1378 | Cite as

Comparative Evaluation of Different Doses of Green Tea Extract Alone and in Combination with Sulfasalazine in Experimentally Induced Inflammatory Bowel Disease in Rats

  • D. S. Prasad Byrav
  • B. Medhi
  • K. Vaiphei
  • A. Chakrabarti
  • K. L. Khanduja
Original Article



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.


Crohn’s disease Ulcerative colitis Tumor necrosis factor Myeloperoxidase Malondialdehyde Interleukin-1 



Analysis of variance


Activator protein


Crohn’s disease


Complementary and alternative medicine


Committee for the Purpose of Control and Supervision on Experiments on Animals


Deoxyribonucleic acid


Epigallocatechin gallate




Epicatechin gallate


Enzyme-linked immunosorbent assay


Green tea






Institutional Animal Ethics Committee


Inflammatory bowel disease






Nuclear factor kappa-light-chain-enhancer of activated B cells


Peroxisome proliferator activated receptor γ


Retinoid X receptor


Standard deviation




Specificity protein


Tumor necrosis factor-α


Tri nitro benzene sulfonic acid




Ulcerative colitis



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. 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. 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. 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
  4. 4.
    Marcel WL. Pharmacological effects of green tea on the gastrointestinal system. Rev Eur J Pharmacol. 2004;500:177–185.CrossRefGoogle Scholar
  5. 5.
    Varilek GW, Yang F, Lee EY, de Villiers WJ, Zhong J, Oz HS. Green tea polyphenol extract attenuates inflammation in interleukin-2-deficient mice, a model of autoimmunity. J Nutr. 2001;131:2034–2039.PubMedGoogle Scholar
  6. 6.
    Yang F, Oz HS, Barve S, de Villiers WJ, McClain CJ, Varilek GW. The green tea polyphenol (-)-epigallocatechin-3-gallate blocks nuclear factor-kappa B activation by inhibiting I kappa B kinase activity in the intestinal epithelial cell line IEC-6. Mol Pharmacol. 2001;60:528–533.PubMedGoogle Scholar
  7. 7.
    Moser G, Tillinger W, Sachs G, et al. Relationship between the use of unconventional therapies and disease-related concerns: a study of patients with inflammatory bowel disease. J Psychosom Res. 1996;40:503–509.PubMedCrossRefGoogle Scholar
  8. 8.
    Hilsden RJ, Scott CM, Verhoef MJ. Complementary medicine use by patients with inflammatory bowel disease. Am J Gastroenterol. 1998;93:697–701.PubMedCrossRefGoogle Scholar
  9. 9.
    Yang F, de Villiers WJ, McClain CJ, Varilek GW. Green tea polyphenols block endotoxin-induced tumor necrosis factor-production and lethality in a murine model. J Nutr. 1998;128(12):2334–2340.PubMedGoogle Scholar
  10. 10.
    Lin YL, Lin JK. Epigallocatechin-3-gallate blocks the induction of nitricoxide synthase by down-regulating lipopolysaccharide-induced activity of transcription factor nuclear factor-B. Mol Pharmacol. 1997;52:465–472.PubMedGoogle Scholar
  11. 11.
    Ryotaro K, Kuroda S, Ohkishi T, Nakamaru K, Hatakeyama S. Oxazolone-induced colitis in BALB/C mice: a new method to evaluate the efficacy of therapeutic agents for ulcerative colitis. J Pharmacol Sci. 2004;96:307–313.CrossRefGoogle Scholar
  12. 12.
    Vogel HG, Goethe JW. Experimental Colitis. Drug discovery and evaluation pharmacological assay. 2nd ed. Germany: Springer; 2002:896–899.CrossRefGoogle Scholar
  13. 13.
    Levine A, Kenet G, Bruck R, et al. Effect of heparin on tissue binding activity of fibroblast growth factor and heparin binding epidermal growth factor in experimental colitis in rats. Pediatric Res. 2002;51:635–640.CrossRefGoogle Scholar
  14. 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. 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. 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. 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
  18. 18.
    Pizarro TT, Michie MH, Bentz M, et al. IL-18, a noval immunoregulatory cytokine, is upregulated in Crohn’s disease: expression and localization in intestinal mucosal cells. J Immunol. 1999;162:6829–6835.PubMedGoogle Scholar
  19. 19.
    Jiao H-L, Ping Y, Zhao B-L. Protective effects of green tea polyphenols on human HepG2 cells against oxidative damage of fenofibrate. Free Radic Biol Med. 2003;35:1121–1128.PubMedCrossRefGoogle Scholar
  20. 20.
    Suske G. The Sp-family of transcription factors. Gene. 1999;238:291–300.PubMedCrossRefGoogle Scholar
  21. 21.
    Pazdrak K, Shi X-Z, Sarna SK. TNF-α suppresses human colonic circular smooth muscle cell contractility by SP1- and NF-κB-mediated induction of ICAM-1. Gastroenterol. 2004;127:1096–1109.CrossRefGoogle Scholar
  22. 22.
    Muller C. Tumour necrosis factor in mouse models of chronic intestinal inflammation. Immunonol. 2002;105:1–8.CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  • D. S. Prasad Byrav
    • 1
  • B. Medhi
    • 1
  • K. Vaiphei
    • 2
  • A. Chakrabarti
    • 1
  • K. L. Khanduja
    • 3
  1. 1.Department of PharmacologyPostgraduate Institute of Medical Education and ResearchChandigarhIndia
  2. 2.Department of HistopathologyPostgraduate Institute of Medical Education and ResearchChandigarhIndia
  3. 3.Department of BiophysicsPostgraduate Institute of Medical Education and ResearchChandigarhIndia

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