ABSTRACT
OBJECTIVE: This study was aimed to investigate the beneficial effects of quercetin (QCT) against trinitrobenzene sulfonic acid (TNBS) induced clinical, morphological, and biochemical alterations in rats. MATERIALS AND METHODS: Colitis in rats was induced by administration of TNBS (25 mg dissolved in 0.25 ml of 30% ethanol) 8 cm into the rectum of the rat using a catheter. The animals were divided into six experimental groups (n = 6); naive (saline only without TNBS administration), control (saline + TNBS), standard (sulfasalazine 25 mg/kg + TNBS), QCT (25) (QCT 25 mg/kg + TNBS), QCT (50) (QCT 50 mg/kg + TNBS), QCT (100) (QCT 100 mg/kg + TNBS). Sulfasalazine (25 mg/kg) and QCT (25, 50 and 100 mg/kg) were administered per oral for 11 days and the colonic damage was evaluated in terms of macroscopical (body weight, stool consistency, rectal bleeding, and ulcer index) and biochemical parameters (myeloperoxidase activity, lipid peroxidation, nitrite, and glutathione). RESULTS: Treatment with QCT (50, 100 mg/kg) for 10 days following TNBS administration significantly attenuated the clinical, morphological, and biochemical alterations induced by TNBS, whereas it was found to be not effective at its lower dose (25 mg/kg) throughout the experimental protocol. CONCLUSION: QCT attenuates the clinical, morphological and biochemical alterations induced by TNBS possibly via its antioxidant mechanism.
Subject(s)
Antioxidants/therapeutic use , Inflammatory Bowel Diseases/drug therapy , Quercetin/therapeutic use , Animals , Antioxidants/pharmacology , Colon/drug effects , Colon/metabolism , Colon/pathology , Glutathione/metabolism , Inflammatory Bowel Diseases/chemically induced , Inflammatory Bowel Diseases/pathology , Lipid Peroxidation/drug effects , Male , Nitrates/blood , Nitrites/blood , Oxidative Stress/drug effects , Quercetin/pharmacology , Rats, Wistar , Trinitrobenzenesulfonic AcidABSTRACT
BACKGROUND: Inflammatory bowel disease (IBD) is characterized by most common symptoms such as rectal bleeding. Lack of specific, curative treatments tempted us to evaluate the therapeutic efficacy of quercetin against acetic acid induced IBD like symptoms. METHODS: Animals were randomly divided into five groups (n = 6): naive, control, sulphasalazine and quercetin, and were pretreated for three days. Colitis was induced by intra-rectal administration of 3% acetic acid. RESULTS: Pretreatment with sulphasalazine or quercetin significantly attenuated the biochemical and morphological alterations in the colon induced by acetic acid in rats. CONCLUSIONS: The findings of the study suggest the possible role of quercetin as therapeutics in IBD.
