AMP-activated protein kinase (AMPK) has been shown to regulate protein metabolism in skeletal muscle. We previously found that levels of Forkhead box proteins, FoxO1 and FoxO3a, and myostatin in rat gastrocnemius increased after exercise-induced muscle damage (EIMD). Eccentric muscle contractions (ECs), defined as elongation of muscle under tension, were used for inducing EIMD. The objective of this study was to clarify whether AMPK participates in activation and expression of FoxO proteins and myostatin in rat gastrocnemius muscle after EIMD. Wistar rats were randomly assigned into the following three groups; CON (n = 6), 180ECs group (ankle angular velocity, 180°/s; n = 6), and 30ECs group (ankle angular velocity, 30°/s; n = 6). 20 ECs were conducted with percutaneous electrical stimulation of gastrocnemius and simultaneous forced dorsiflexion of ankle joint (from 0° to 45°). To evaluate activation of AMPK, we measured the phosphorylated states of AMPK and acetyl CoA carboxylase. For evaluation of the direct relationships of AMPK and other proteins, we also examined contents of FoxOs and myostatin with stimulation of L6 myotube with AMPK agonist, 5 -aminoimidazole -4 -carboxamide -1-β-d-ribofuranoside (AICAR) (0.1, 0.5, 1, 1.5, and 2 mM). Western blotting was employed for protein analysis. Significant torque deficit was only observed in the 180ECs, suggesting EIMD. We also observed that phosphorylated AMPKα was induced in response to 180ECs (p < 0.01 vs. CON). Additionally, the level of phosphorylated acetyl CoA carboxylase was significantly higher in response to 180ECs and 30ECs. The phosphorylated states of FoxO1, FoxO3a, and myostatin expression were increased significantly in response to 180ECs. Furthermore, treatment of L6 myotubes with AICAR showed similar tendencies to that observed in in vivo gastrocnemius muscle treated with 180ECs. Therefore, we conclude that activation of AMPK plays a key role in increasing the level of FoxO1, FoxO3a, and myostatin in gastrocnemius after EIMD.

译文

:AMP激活的蛋白激酶(AMPK)已被证明可调节骨骼肌中的蛋白代谢。我们以前发现运动诱发的肌肉损伤(EIMD)后,大鼠腓肠肌中Forkhead box蛋白,FoxO1和FoxO3a和肌生长抑制素的水平增加。偏心肌收缩(ECs)定义为在张力下的肌肉伸长,用于诱发EIMD。这项研究的目的是阐明EIMD后AMPK是否参与大鼠腓肠肌中FoxO蛋白和肌肉生长抑制素的激活和表达。 Wistar大鼠随机分为以下三组: CON(n = 6),180ECs组(踝角速度,180°/ s; n = 6)和30ECs组(踝角速度,30°/ s; n = 6)。在经皮电刺激腓肠肌并同时强迫踝关节背屈(0°至45°)的情况下进行20个EC。为了评估AMPK的激活,我们测量了AMPK和乙酰辅酶A羧化酶的磷酸化状态。为了评估AMPK与其他蛋白质的直接关系,我们还检查了AMPK激动剂5-氨基咪唑-4-甲酰胺-1-β-d-核呋喃核苷(AICAR)刺激L6肌管后FoxOs和肌生长抑制素的含量0.5、1、1.5和2 mM)。 Western印迹用于蛋白质分析。仅在180EC中才观察到明显的扭矩不足,提示为EIMD。我们还观察到磷酸化的AMPKα是在响应180ECs时被诱导的(p <0.01 vs.CON)。另外,响应180EC和30EC,磷酸化的乙酰辅酶A羧化酶的水平明显更高。 FoxO1,FoxO3a和肌生长抑制素表达的磷酸化状态响应180ECs显着增加。此外,用AICAR治疗L6肌管的趋势与在用180ECs治疗的体外腓肠肌中观察到的趋势相似。因此,我们得出结论,EIMD后AMPK的激活在腓肠肌增加FoxO1,FoxO3a和肌生长抑制素的水平中起着关键作用。

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