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目的探讨线粒体融合蛋白2(Mfn2)是否通过减轻氧化应激改善大鼠骨骼肌细胞IR。方法建立高脂诱导骨骼肌细胞IR模型(PA组),以Mfn2基因重组腺病毒转染细胞(PMfn2组),观察细胞内葡萄糖摄取率、超氧化物歧化酶总活力(T-SOD)、过氧化氢酶(CAT)、活性氧簇(ROS)及MDA的改变。结果 (1)与正常对照(NC)组相比,高脂(PA)组葡萄糖摄取率降低(P<0.01),T-SOD及CAT活性降低,ROS、MDA含量增加(P<0.05);(2)与PA组相比,Mfn2基因重组腺病毒转染(PMfn2)组T-SOD及CAT活力均增加(P<0.05);ROS水平、MDA含量降低(P<0.05);GSH-Px活力无明显改变。结论上调高脂干预后骨骼肌细胞的Mfn2水平可减轻细胞氧化应激,改善IR。
Objective To investigate whether mitochondrial fusion protein 2 (Mfn2) improves the IR of rat skeletal muscle cells by reducing oxidative stress. Methods High glucose-induced IR model of skeletal muscle cells (PA group) was established. The Mfn2 recombinant adenovirus transfected cells (PMfn2 group) were established. The intracellular glucose uptake, the activity of superoxide dismutase (T-SOD) Catalase (CAT), reactive oxygen species (ROS) and MDA changes. Results Compared with normal control group, glucose uptake in the high fat diet group decreased (P <0.01), T-SOD and CAT activity decreased, ROS and MDA contents increased (P <0.05); ( 2) Compared with PA group, the activities of T-SOD and CAT in Mfn2 gene-transfected PMFn2 group were increased (P <0.05); ROS level and MDA content were decreased (P <0.05); the activity of GSH-Px Significant change. Conclusion Upregulation of Mfn2 in skeletal muscle cells induced by high fat diet can reduce cellular oxidative stress and improve IR.