title: Comparative evaluation of different doses of green tea extract alone and in combination with sulfasalazine in experimentally induced inflammatory bowel disease in rats.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  The authors concluded that a combination of green tea extract with sulfasalazine showed greater efficacy than single drug treatment.
authors.affiliation: Department of Pharmacology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. drbikashus@yahoo.com
authors.forename: D S Prasad
authors.initials: DS
authors.lastname: Byrav
authors.forename: B
authors.initials: B
authors.lastname: Medhi
authors.forename: K
authors.initials: K
authors.lastname: Vaiphei
authors.forename: A
authors.initials: A
authors.lastname: Chakrabarti
authors.forename: K L
authors.initials: KL
authors.lastname: Khanduja
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000627:therapeutic use; D028241:Camellia sinensis / Q000737:chemistry*; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D005260:Female; D015212:Inflammatory Bowel Diseases / Q000139:chemically induced* / Q000188:drug therapy*; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D010936:Plant Extracts / Q000008:administration & dosage / Q000737:chemistry* / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D012460:Sulfasalazine / Q000008:administration & dosage / Q000627:therapeutic use*; D014302:Trinitrobenzenesulfonic Acid / Q000633:toxicity; D014409:Tumor Necrosis Factor-alpha
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; D012460:Sulfasalazine; D008315:Malondialdehyde; D014302:Trinitrobenzenesulfonic Acid; D009195:Peroxidase