CAJ | 학술논문

Background:Ulcerative colitis(UC)is a chronic and nonspecific intestinal inflammatory disease and its pathogenic mechanism has not yet been clarified. Intestinal mucosal immune function disorder may play a key role in the pathogenesis of UC. Aims:To investigate the effects of Wumeiwan on expressions of δ-opioid receptor(DOR),β-arrestin1 and Bcl-2 in rats with colitis. Methods:Fifty-six Sprague-Dawley rats were randomly divided into model group,Wumeiwan group, mesalazine group and blank group. Rats in model group,Wumeiwan group and mesalazine group were administered intrarectally with 5% TNBS and 50% ethanol to induce experimental colitis. After colitis models were established,rats in Wumeiwan group and mesalazine group were administered intragastrically with Wumeiwan and mesalazine suspension, respectively,and rats in model group and blank group were given intragastrically with 0. 9% NaCl solution,all for 15 days. On day 16,all the rats were sacrificed and colon samples were obtained. Protein and mRNA expressions of DOR,β-arrestin1 and Bcl-2 in colonic tissue were determined by immunohistochemistry and real-time PCR,respectively. Results:The inflammatory injury in colonic tissue of rats with experimental colitis was significantly attenuated when treated with Wumeiwan,Protein and mRNA expressions of DOR,β-arrestin1 and Bcl-2 in colonic tissue of model group were significantly higher than those of blank group(P < 0. 05). Protein and mRNA expressions of DOR,β-arrestin1 and Bcl-2 in colonic tissue of Wumeiwan group and mesalazine group were significantly lower than those of model group(P < 0. 05), however,no significant differences were found between the two groups(P > 0. 05). Conclusions:DOR-β-arrestin1-Bcl-2 signal transduction pathway may play a central role in the pathogenesis of UC. Intervening this signaling pathway may be one of the mechanisms of attenuating UC by Wumeiwan.