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Updated: Jun 6, 2026

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
Published on: February 27, 2014
Effects of recombinant human intestinal trefoil factor on trinitrobenzene sulphonic acid induced colitis in rats
Jin Li1, Rui Zhou, Wen-Cheng He
1Department of Gastroenterology, Zhongnan Hospital of Wuhan University, Hubei Provincial Center of Clinical Study for Intestinal & Colonrectal Disease, Donghu Road 169, Wuhan 430071, Hubei Province, People's Republic of China. lijinluyi@gmail.com
Abstract:
Intestinal trefoil factor (ITF) has been proved to be effective in treatment of ulcerative colitis. However, the mechanisms of it remain unclear. In this study, we observed the effects of combined treatment with 5-aminosalicylic acid (5-ASA) and recombinant human ITF (rhITF) on the expression of Myeloperoxidase (MPO), nuclear factor-κB (NF-κB) and epidermal growth factor (EGF) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats. Forty Sprague-Dawley (SD) male rats which were induced to distal colitis by the colonic administration of TNBS, were randomly divided into four groups and colonically treated with normal saline (A), 5-ASA (B), rhITF (C), respectively. The macroscopic and histological changes of the colon, activities of MPO, expressions of serum EGF and tissue NF-κB were detected. The results showed that manifestation, colonic damage score and MPO activities of the rats treated with 5-ASA or/and rhITFs were improved, serum EGF production was augmented and expression of tissue NF-κB was down-regulated. Single usage of 5-ASA or rhITF had no significant difference, but combined using of them had more significant and noticeable effects compared to any single treatment. It could be concluded that topical treatment with 5-ASA and rhITF had beneficial effects in treating TNBS-induced colitis of rats and combined treatment was better than single treatment. It was possibly related to suppression of neutrophil infiltration, down-regulation expression of NF-κB and up-regulation expression of EGF.

