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目的探讨糖尿病大鼠骨骼肌氧化应激水平及其对肌特异性环指蛋白1基因(MuRF1)表达的影响。方法通过高糖高脂饮食联合尾静脉注射链脲佐菌素(STZ)构建2型糖尿病大鼠模型,分别检测大鼠腓肠肌肌纤维面积、脂质过氧化水平、超氧化物歧化酶(SOD)活性以及MuRF1 mRNA的表达水平,同时设对照组;通过体外培养C2C12成肌细胞,不同浓度H2O2(0、0.01、0.05、0.10和0.20 mmol/L)诱导肌管细胞内氧化应激,Westernblot检测不同程度氧化应激下细胞MuRF1的表达水平。结果与对照组大鼠相比较,糖尿病大鼠腓肠肌肌纤维面积减小,脂质过氧化水平增高,MuRF1 mRNA表达上调(P<0.01);体外细胞培养发现0.05、0.10、0.20 mmol/LH2O2诱导的C2C12肌管细胞氧化应激可上调MuRF1的表达(P<0.01)。结论糖尿病大鼠骨骼肌氧化应激水平增高,使MuRF1基因表达上调,从而导致骨骼肌萎缩。
Objective To investigate the oxidative stress in skeletal muscle of diabetic rats and its effect on the expression of muscle specific loop finger protein 1 (MuRF1). Methods The model of type 2 diabetes mellitus was established by injecting streptozotocin (STZ) into the tail vein of high glucose and high fat diet. The muscle fiber area, lipid peroxidation, superoxide dismutase (SOD) activity, And the expression of MuRF1 mRNA in the control group. The C2C12 myoblasts were cultured in vitro, and the oxidative stress was induced by different concentrations of H2O2 (0, 0.01, 0.05, 0.10 and 0.20 mmol / L) Oxidative stress in cells MuRF1 expression levels. Results Compared with the control group, the area of muscle fiber of gastrocnemius and the level of lipid peroxidation were increased in diabetic rats and the expression of MuRF1 mRNA was up-regulated (P <0.01). In vitro cultured cells were found to have 0.05, 0.10 and 0.20 mmol / L H2O2 induced C2C12 Oxidative stress in myotubes increased the expression of MuRF1 (P <0.01). Conclusion The oxidative stress in skeletal muscle of diabetic rats is increased, and the expression of MuRF1 gene is up-regulated, resulting in skeletal muscle atrophy.