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[目的]研究α-硫辛酸对2型糖尿病大鼠氧化应激致胰岛细胞凋亡的影响。[方法]采用高热量饮食联合腹腔注射低剂量链脲菌素制备2型糖尿病大鼠模型(模型对照组),予以α-硫辛酸(15、30、60和120 mg/kg体质量)干预处理12周后,检测大鼠胰腺组织氧化应激指标和胰岛细胞凋亡情况,同时检测胰腺组织中凋亡相关蛋白的表达改变。[结果]与模型组相比,各干预组大鼠胰腺组织中丙二醛含量均明显降低(P<0.01),总超氧化物歧化酶和谷胱甘肽过氧化物酶活性则明显升高(P<0.01);除15 mg/kg体质量组外,其余各干预组大鼠胰岛凋亡指数较模型组均明显降低(P<0.01),其中以60 mg/kg体质量干预组效果最好。与模型组比较,各干预组大鼠胰腺组织中Bax、Fas、活化型Caspase-9和Caspase-3等蛋白表达均降低,而Bcl-2蛋白表达则明显增高。[结论]α-硫辛酸可通过调节大鼠胰腺组织的氧化应激状态,改变凋亡相关蛋白的表达水平,显著降低2型糖尿病模型大鼠胰岛细胞的凋亡率,增加机体胰岛素的分泌水平。
[Objective] To investigate the effect of α-lipoic acid on the apoptosis of islet cells induced by oxidative stress in type 2 diabetic rats. [Method] A rat model of type 2 diabetes mellitus (model control group) was prepared by intraperitoneal injection of high caloric diet combined with low dose of streptozotocin. The rats were treated with a-lipoic acid (15, 30, 60 and 120 mg / kg body weight) After 12 weeks, the rat pancreatic tissue oxidative stress indicators and pancreatic islet cell apoptosis were detected, and the expression of apoptosis-related proteins in pancreatic tissues was also detected. [Results] Compared with the model group, the contents of malondialdehyde in the pancreas of the intervention groups were significantly decreased (P <0.01) and the activities of total superoxide dismutase and glutathione peroxidase were significantly increased (P <0.01). Compared with the model group, the apoptotic index of all intervention groups except 15 mg / kg body weight group was significantly lower than that of the model group (P <0.01), and the effect of 60 mg / kg body weight intervention group it is good. Compared with the model group, the protein expressions of Bax, Fas, activated Caspase-9 and Caspase-3 in the pancreas of each intervention group were decreased, while the Bcl-2 protein expression was significantly increased. [Conclusion] α-lipoic acid can change the expression of apoptosis-related protein by regulating the oxidative stress in rat pancreatic tissue and significantly decrease the apoptosis rate of pancreatic islet cells and increase the level of insulin secretion in type 2 diabetic rats .