Exercise training has beneficial anti-atrophy effects by inhibiting oxidative stress-induced MuRF1 upregulation in rats with diabetes

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• 作者：Guo-Qing Chen^a ; Cai-Ying Mou^a ; Yue-Qin Yang^a ; Song Wang^a ; Zhi-Wei Zhao^b ; ^{zhiwzhao@163.com"" rel=""nofollow}
• 关键词：Diabetes ; Skeletal muscle atrophy ; Oxidative stress ; MuRF1
• 刊名：Life Sciences
• 出版年：2011
• 出版时间：4 July 2011
• 年：2011
• 卷：89
• 期：1-2
• 页码：44-49
• 全文大小：522 K

文摘

Aims

MuRF1 E3 ubiquitin ligase has been identified as a mediator of skeletal muscle wasting in various skeletal muscle atrophy models, and its expression is upregulated by oxidative stress. Exercise training could decrease oxidative stress and restore the atrophied skeletal muscle. Here, our aim was to investigate whether exercise training has any effect on MuRF1 expression in rats with diabetes.

Main methods

Rats with streptozotocin-induced diabetes were subjected to exercise training, after which oxidative stress was determined, and MuRF1 expression was analyzed by immunohistochemistry, real-time RT-PCR and Western blot analysis. In addition, we analyzed C2C12 myotubes in an in vitro model to examine the effects of oxidative stress on the protein levels of MuRF1 and myosin heavy chain (MHC).

Key findings

While oxidative stress and MuRF1 expression were increased in rats with diabetes, exercise training diminished the skeletal muscle wasting in diabetic rats by decreasing oxidative stress and inhibiting MuRF1 expression at both the mRNA and protein levels. In addition, oxidative stress-induced MuRF1 upregulation promoted proteasome dependent degradation of the myosin heavy chain (MHC) in C2C12 myotubes.

Significance

Our study provides the first evidence that the beneficial anti-atrophy effects of exercise training on diabetes might be mediated by inhibiting oxidative stress-induced MuRF1 upregulation and preventing MuRF1-mediated degradation of MHC.