Mechanism of Oxymatrine Alleviating Oxidative Damage of Colonic Mucosal Cells by Regulating Autophagy in Ulcerative Colitis Mice

OBJECTIVE To investigate the mechanism of oxymatrine reducing oxidative damage of colonic mucosal via controlling cell autophagy ulcerative colitis(UC) mice. METHODS UC model was induced by 2,4,6-trinitrobenzenesulfonic acid. Mice of successful model were randomly divided into model group, oxymatrine group(50 mg·kg^-1·d^-1, ig), hydroxychloroquine group(50 mg·kg^-1·d^-1, ig) and oxymatrine + hydroxychloroquine group of 10 animals in each group, normal group was also set. One week after the treatment, the disease activity(DAI), the colon weight index and pathomorphology were determined; the colon ROS content was determined by MitoSOX Red method; the contents of SOD, MDA, MPO and GSH-PX in the colon tissues were determined by ELISA method; the degree of autophagy of colonic cells was observed by electron microscope and immunofluorescence; the expression of Atg5 and Beclin-1 proteins were detected by Western blot. RESULTS Compared with the model group and the hydroxychloroquine group, the DAI and the colonic weight index of oxymatrine group were significantly decreased(P<0.01), and the colonic pathological damage was significantly reduced; the contents of ROS, MDA and MPO were significantly decreased(P<0.01); the contents of SOD and GSH-PX were significantly increased(P<0.01). The degree of autophagy in colonic mucosa was significantly increased, and the expressions of Atg5 and Beclin-1 were significantly upregulated(P<0.01). CONCLUSION Oxymatrine can reduce the oxidative damage of colonic mucosa by promoting autophagy in UC mice.