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目的探讨线粒体氧化应激(MOS)在糖尿病心肌病(DCM)发生发展中的作用和α-硫辛酸(α-LA)保护机制。方法大鼠分为正常对照(NC)组,糖尿病(DM)组,糖尿病α-LA治疗组(α-LA组)。4、8、12周末测定大鼠心功能、心脏胶原含量、线粒体谷胱甘肽(GSH)、MDA含量和Mn-SOD的活性,镜下观察心脏病理改变。结果随病程延长,DM组大鼠心功能受损加重、胶原含量增加,病理改变加重,心肌线粒体Mn-SOD的活性和GSH的含量下降,MDA的含量明显上升;α-LA治疗后能够显著逆转糖尿病大鼠上述指标的变化。MDA与心脏胶原含量呈正相关。结论糖尿病大鼠MOS与DCM发生发展密切相关,α-LA通过升高心肌线粒体Mn-SOD活性和GSH的含量减弱MOS损伤保护DCM。
Objective To investigate the role of mitochondrial oxidative stress (MOS) in the development of diabetic cardiomyopathy (DCM) and the mechanism of α-lipoic acid (α-LA) protection. Methods The rats were divided into normal control (NC) group, diabetes mellitus (DM) group and diabetic α-LA treatment group (α-LA group). Cardiac function, cardiac collagen content, glutathione (GSH), MDA content and Mn-SOD activity were measured at 4,8,12weeks. The pathological changes were observed under microscope. Results With the prolongation of duration, cardiac function was impaired, collagen content was increased, the pathological changes were aggravated, the activity of mitochondrial Mn-SOD and the content of GSH were decreased and the content of MDA was significantly increased in DM group. Changes of the above indexes in diabetic rats. MDA and cardiac collagen content was positively correlated. Conclusion MOS in diabetic rats is closely related to the occurrence and development of DCM. Α-LA protects DCM by increasing the activity of Mn-SOD and the content of GSH in myocardial mitochondria.