at a dose of 100 mg/kg b.wt. inhibited the DNCB-induced overexpression of NFκ-B and iNOS in the colon. CONCLUSION:Curcumin treatment ameliorates colonic damage in DNCB-induced colitic rats, an effect associated with an improvement in intestinal oxidative stress and downregulation of colonic NFκ-B and iNOS expression. INTRODUCTIONInflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis (UC), is a chronic and relapsing inflammatory disease caused by the inflammation and sores in the lining of large intestine and characterized clinically by recurrent episodes of bloody diarrhea, cramping, abdominal pain and histologically by mucosal inflammation and injury [1] . Conventional therapy for UC includes sulfasalazine and other 5-aminosalicylic acid (5-ASA) type of compounds, and in more persistent and/ or severe cases, oral, rectal and parenteral corticosteroids and immunosuppressants are administered [2] . All of these have significant toxicities and are partly or completely ineffective in significant numbers of patients [3] . Several agents used in the management of IBD, such as corticosteroids, sulfasalazine and 5-ASA, have documented regulation of Nuclear Factor K appa-B (NF κ-B) function [2] . Given the importance of inflammatory cell activation involved in the development of IBD, there is a need for a treatment modality against IBD that can block the inflammatory processes. There is substantial evidence for the involvement of oxidative stress and profound alterations in the biosynthesis of the labile free Abstract AIM: To evaluate the efficacy and mechanism of action of NCB-02, a standardized Curcumin preparation, against 2, 4-dinitrochlorobenzene (DNCB)-induced ulcerative colitis in rats.

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