OBJECTIVETo investigate the pathogenetic mechanism of beta-arrestin1 in the rat's experimental colitis, whether the delta opioid receptor-beta-arrestin1 -Bcl-2 signal transduction pathway involves the pathological process of experimental colitis in rats, and whether oxymatrine could attenuate colitis through this pathway.

METHODSTwenty-six SD rats were randomly divided into four groups, the normal control group, the model group, the mesalazine treated group and the oxymatrine treated group (8 rats in the last group and 6 each in the others). The colitis model was established with trinitrobenzene sulfonic acid (TNBS), and rats in the latter two groups were treated by oxymatrine (intramuscular injection) and mesalazine (3 mL solution gavaged) for 15 days, respectively, while rats in the former two groups were fed with equal volume of distilled water. Symptoms of diarrhea and bloody stool as well as colonic patho-histologic changes were observed, and changes in expressions of delta opioid receptor, beta-arrestin1 and Bcl-2 in rat's colon tissue and spleen T lymphocytes were detected with immuno-histochemistry and Western immune-blotting techniques, respectively.

RESULTSIn contrast to the normal control group, expressions of delta opioid receptor, beta-arrestin1 and Bcl-2 were significantly higher in the model group (P < 0.01); compared with the model group, they were significantly lower in the two treated groups (P < 0.01).

CONCLUSIONSDelta opioid receptor-beta-arrestin1 -Bcl-2 signal transduction pathway participates in the pathogenesis of TNBS-induced experimental colitis in rats. Oxymatrine can intervene the signal transduction, which may be one of the mechanisms of oxymatrine in attenuating colitis in rats.