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目的研究血管紧张素1-7[Ang-(1-7)]在骨骼肌细胞糖代谢中的作用。方法原代提取C57小鼠成肌细胞,诱导分化为成熟细胞,分别予Ang-(1-7)及A779干预,采用非同位素法检测2-脱氧葡萄糖摄取率,氯化硝基四氮唑蓝(NBT)染色法检测细胞内活性氧簇(ROS)含量,RT-PCR检测氧化应激相关基因表达;用Ang-(1-7)干预糖尿病大鼠(OLETF),Western blot检测骨骼肌组织胰岛素信号通路蛋白表达。结果 Ang-(1-7)增加原代培养的骨骼肌细胞葡萄糖摄取和骨骼肌pIRS-1(tyr1179)、pAkt(ser473)的蛋白表达,降低骨骼肌细胞中ROS的产生和还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)亚基p22、NOX1的表达。结论 Ang-(1-7)可改善骨骼肌糖代谢,其作用机制可能与改善骨骼肌氧化应激有关。
Objective To investigate the role of angiotensin 1-7 [Ang- (1-7)] in glycometabolism in skeletal muscle cells. Methods Primary myoblasts of C57 mice were induced and induced to differentiate into mature cells. The cells were treated with Ang- (1-7) and A779 respectively. The uptake of 2-deoxyglucose, the absorption rate of nitroblue tetrazolium chloride (ROS) was measured by NBT staining, and the expression of oxidative stress-related genes was detected by RT-PCR. Angiotensin II (1-7) was used to detect the expression of insulin in skeletal muscle tissue of diabetic rats (OLETF) Signal pathway protein expression. Results Ang- (1-7) increased glucose uptake in primary cultured skeletal muscle cells and protein expression of pIRS-1 (tyr1179) and pAkt (ser473) in skeletal muscle, decreased ROS production in skeletal muscle cells and reduced nicotinamide adenine Purine dinucleotide phosphate (NADPH) subunit p22, NOX1 expression. Conclusion Ang- (1-7) can improve the metabolism of skeletal muscle glucose, the mechanism may be related to the improvement of skeletal muscle oxidative stress.