RESUMEN
Objective To explore the specific mechanism by which estrogen affects the inflammatory bowel disease (IBD) in rats. Methods The model of IBD in rats was established with 30% of 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) ethanol solution through the rectocolon. The body weight, disease activity index(DAI) score, colorectal length, myeloperoxidase (MPO) concentration, and H-E staining were used to verify the successful IBD model. The IBD rats were separately treated with saline(500 μL), estrogen(1 mg/kg,in 500 μL normal saline), and PPT, a specific agonist of estrogen receptor alpha (ERα; 3 mg/kg, in 500 μL normal saline), or estrogen(1 mg/kg,in 500 μL normal saline) + ERα specific antagonist MPP(3 mg/kg, in 500 μL normal saline). And the inflammation status was observed. Results The model of IBD in rats was successfully induced by TNBS. Compared with the normal saline group, rats in TNBS group had significantly reduced body weight and increased DAI scores, with MPO value increased and with notable inflammatory response of the rectocolon. Compared with normal saline group, estrogen or PPT significantly aggravated the inflammation response. Estrogen treatment significantly reduced the body weight of IBD rats, increased DAI scores, and aggravated the inflammatory response, with the colorectal length reduced; PPT reduced the colorectal length. MPP treatment reversed the effect of estrogen. Compared with the estrogen group, MPP+estrogen treatment significantly increased the body weight and reduced the DAI scores, with colorectal length increased. Conclusion Estrogen can promote the development and progression of TNBS-induced IBD, which might be mediated through ERα.