Insulin-like Growth Factor-I Partially Attenuates Colonic Damage in Rats with Experimental Colitis Induced by Oral Dextran Sulphate Sodium

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Abstract
Administration of insulin-like growth factor-I (IGF-I) results in selective growth of the gastrointestinal tract. We investigated the effects of IGF-I on the colonic damage induced by oral dextran sulphate sodium (DSS) in the rat. Rats consumed 2% DSS in the drinking water for 10 days to induce colitis. Pumps were implanted on day 3 to deliver IGF-I for 7 days. Colonic histopathology and immunolocalization of transforming growth factor-beta1 (TGF-beta1) were assessed on day 10. Compared with the colon of vehicle-treated rats consuming DSS, IGF-I increased the numbers of goblet cells by 76%, reduced the proportion of lamina propria cells expressing TGF-beta1, and reduced the thickness of submucosal and muscularis externa layers by 26% and 20%, respectively. We conclude that the effects of IGF-I treatment on the colonic epithelium may be mediated directly, whereas the reduced inflammation in the mucosa and submucosa may be mediated by a mechanism other than up-regulation of TGF-beta1-mediated immunosuppression.