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目的探讨OLETF大鼠骨骼肌的氧化应激和Bcl-xL表达及罗格列酮(RGZ)的干预效应。方法设LETO大鼠为正常对照(NC)组,OLETF大鼠分为RGZ组和糖尿病(DM)组,测骨骼肌组织中一氧化氮(NO)、总超氧化物歧化酶(T-SOD)、谷胱甘肽(GSH)和丙二醛(MDA),对骨骼肌细胞Bcl-xL表达情况进行检测。结果与NC组相比,DM组骨骼肌组织中NO、T-SOD、GSH和骨骼肌细胞Bcl-xL阳性表达强度降低(P<0.05或P<0.01),MDA升高(P<0.01);RGZ组相对于DM组NO、T-SOD和Bcl-xL阳性表达强度升高(P<0.01),MDA降低(P<0.05)。结论 T2DM本身可能通过促进骨骼肌组织氧化损伤加重细胞凋亡,而罗格列酮可能通过降低其氧化损伤缓解骨骼肌细胞凋亡,对骨骼肌有保护作用。
Objective To investigate the oxidative stress and the expression of Bcl-xL in skeletal muscle of OLETF rats and the effect of rosiglitazone (RGZ) on it. Methods LETO rats were divided into normal control group (NC) and OLETF rats. The OLETF rats were divided into RGZ group and DM group. The levels of nitric oxide (NO), total superoxide dismutase (T-SOD) , Glutathione (GSH) and malondialdehyde (MDA) were measured to detect the expression of Bcl-xL in skeletal muscle cells. Results Compared with NC group, the expression of NO, T-SOD, GSH and Bcl-xL in skeletal muscle of DM rats decreased (P <0.05 or P <0.01) and MDA increased (P <0.01) The expressions of NO, T-SOD and Bcl-xL in RGZ group were significantly higher than those in DM group (P <0.01), and MDA levels were lower (P <0.05). Conclusion T2DM itself may promote apoptosis by promoting the oxidative damage of skeletal muscle tissue, while rosiglitazone might protect skeletal muscle cells by decreasing its oxidative damage and relieving skeletal muscle cell apoptosis.