中文摘要：

目的研究PI3K/AKT/mTOR信号通路在慢性阻塞性肺疾病（简称慢阻肺）大鼠骨骼肌萎缩中的作用。方法采用单纯熏香烟法复制慢阻肺大鼠动物模型。采用Western blot技术检测慢阻肺大鼠趾长伸肌中PI3K/AKT/mTOR信号通路中PI3K、总的及磷酸化的mTOR（t-mTOR,p-mTOR）、总的及磷酸化的GSK-3β（t-GSK-3β,p-GSK-3β）、总的及磷酸化的4E-BP1（t-4E-BP1,p-4E-BP1）、总的及磷酸化的p70S6K1（t-p70S6K1,p-p70S6K1）蛋白表达变化。结果 Western blot分析结果显示,大鼠趾长伸肌组织中PI3K的蛋白表达在两组间差异不显著（P〉0.05）;t-mTOR、p-mTOR、t-GSK-3β和p-GSK-3β的蛋白表达慢阻肺组显著高于对照组（P〈0.05,其中p-GSK-3β两组对照P〈0.01）;t-4E-BP1和t-p70S6K1的蛋白表达在两组间差异不显著（P〉0.05）,p-4E-BP1和p-p70S6K1的蛋白表达慢阻肺组显著高于对照组（P〈0.05）。结论慢阻肺大鼠趾长伸肌组织内PI3K/AKT/mTOR信号通路被激活,可能是骨骼肌萎缩的代偿机制之一。

英文摘要：

Objective To investigate the role of PI3K/AKT/mTOR signaling pathway in skeletal muscle atrophy in rats with chronic obstructive pulmonary diseases（ COPD）. Methods Passive cigarette smoking was used to establish COPD model. The protein expression of PI3 K,total mTOR,phosphorylatedmTOR,total GSK-3β,phosphorylated-GSK-3β,total 4E-BP1,phosphorylated-4E-BP1,total p70S6K1 and phosphorylated-p70S6K1 in extensor digitorum longus of rats were measured by Western blot. Results The protein expression of PI3 K was not significantly different between two groups（ P 〉 0. 05）. Compared with the control group,the protein expression of total mTOR,phosphorylated-mTOR,total GSK-3β,and phosphorylated-GSK-3β increased significantly in the COPD group（ P 〈 0. 05）. The protein expression of total 4E-BP1 and total p70S6K1 were not significantly different between two groups（ P 〉 0. 05）. While the protein expression of phosphorylated-4E-BP1 and phosphorylated-p70S6K1 significantly increased in the COPD group（ P 〈 0. 05）. Conclusion The protein expressions of PI3 K /AKT /mTOR signaling pathway in extensor digitorum longus increased significantly in COPD rats,suggesting that the activity of PI3 K /AKT /mTOR signaling pathway increased,which may be one of the compensatory mechanism of skeletal muscle atrophy in COPD.