PDF(Pubmed)
Abstract：
OBJECTIVE: This study investigated the effects of resistance exercise on the Akt-eNOS, the activation of antioxidant protein and FOXO1 in the aorta of F344 rats.
METHODS: Male 7 week-old F344 rats were randomly divided into 2 groups: a climbing group (n = 6) and a sedentary group (n = 6). H&E staining and western blotting were used to analyze the rat aortas and target proteins.
RESULTS: Resistance exercise training did not significantly affect aortic structure. Phosphorylation of AKT and eNOS and expression of MnSOD and Ref-1 were significantly increased while FOXO1 phosphorylation was significantly decreased in the resistance exercise group compared with the sedentary group.
CONCLUSIONS: We demonstrate that resistance exercise activates the Akt-eNOS and Ref-1 protein without changes to aortic thickness via FOXO-1 activation in the aorta of F344 rats.
METHODS: Male 7 week-old F344 rats were randomly divided into 2 groups: a climbing group (n = 6) and a sedentary group (n = 6). H&E staining and western blotting were used to analyze the rat aortas and target proteins.
RESULTS: Resistance exercise training did not significantly affect aortic structure. Phosphorylation of AKT and eNOS and expression of MnSOD and Ref-1 were significantly increased while FOXO1 phosphorylation was significantly decreased in the resistance exercise group compared with the sedentary group.
CONCLUSIONS: We demonstrate that resistance exercise activates the Akt-eNOS and Ref-1 protein without changes to aortic thickness via FOXO-1 activation in the aorta of F344 rats.
摘要：
目的：本研究探讨了抗阻运动对Akt-eNOS的影响，F344大鼠主动脉中抗氧化蛋白和FOXO1的激活。
方法:7周龄雄性F344大鼠随机分为2组:攀爬组(n=6)和久坐组(n=6)。使用H&E染色和蛋白质印迹法分析大鼠主动脉和靶蛋白。
结果：阻力运动训练对主动脉结构没有显著影响。与久坐组相比，抵抗运动组AKT和eNOS的磷酸化以及MnSOD和Ref-1的表达显着增加，而FOXO1的磷酸化显着降低。
结论：我们证明阻力运动激活Akt-eNOS和Ref-1蛋白，而不会通过F344大鼠主动脉中的FOXO-1激活而改变主动脉厚度。
方法:7周龄雄性F344大鼠随机分为2组:攀爬组(n=6)和久坐组(n=6)。使用H&E染色和蛋白质印迹法分析大鼠主动脉和靶蛋白。
结果：阻力运动训练对主动脉结构没有显著影响。与久坐组相比，抵抗运动组AKT和eNOS的磷酸化以及MnSOD和Ref-1的表达显着增加，而FOXO1的磷酸化显着降低。
结论：我们证明阻力运动激活Akt-eNOS和Ref-1蛋白，而不会通过F344大鼠主动脉中的FOXO-1激活而改变主动脉厚度。
