【摘要】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胰岛素抵抗模型(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)与正常对照组(NC组)相比，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，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。

　　【关键词】骨骼肌细胞;胰岛素抵抗;Mfn2;氧化应激;大鼠

　　【Abstract】 Objective To study whether the mitofusin 2 (Mfn2) improves insulin resistance (IR) in skeletal muscle cells of rats via reduction of oxidative stress. Methods High fat-induced insulin resistance model in skeletal muscle cells was established (PA group), with Mfn2 genetic recombination adenovirus transfecting cells (PMfn2 group), and changes of intracellular glucose uptake rate, the total activity of superoxide dismutase (T-SOD), catalase (CAT), reactive oxygen species (ROS) and MDA were observed. Results (1) Compared with the normal control group (NC group), glucose uptake rate of PA group was decreased (P < 0.01), T-SOD and CAT activities were reduced, and the contents of ROS and MDA were increased (P < 0.05); (2) Compared with the PA group, T-SOD and CAT activities of PMfn2 group were increased (P < 0.05); ROS levels and MDA content were decreased (P < 0.05); and GSH-Px activity had no significant change. Conclusions To increase the Mfn2 level in skeletal muscle cells by intervention of high fat can reduce cellular oxidative stress, and improve IR.

　　【Key words】Skeletal muscle cells; Insulin resistance; Mfn2; Oxidative stress; Rats