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[高负荷运动诱导大鼠骨骼肌损伤对自噬超微结构及Beclin1和LC3-II/I的影响]

[Effects of high-load exercise induced skeletal muscle injury on autophagy ultrastructure and Beclin1 and LC3-II / I in rats].

作者信息

Zhang Xin, Wang Rui-Yuan

机构信息

School of Sport and Health, Nanjing Sport Institute, Nanjing 210014.

Sport Science College, Beijing Sport University, Beijing 100084, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2020 Jul;36(4):296-300. doi: 10.12047/j.cjap.5944.2020.064.

DOI:10.12047/j.cjap.5944.2020.064
PMID:33167086
Abstract

OBJECTIVE

To investigate the effects of high-load eccentric exercise on the ultrastructure of autophagy and the autophagy-related proteins Beclin1 and LC3II / I in rats.

METHODS

Forty-eight SD male rats were randomly divided into control group (C, =8) and high-load eccentric exercise group (E, =40) after adaptive training. Group E was run downhill for 90 minutes on the running platform, and soleus muscles were collected at 0, 12, 24, 48 and 72 hours after exercise. Transmission electron microscopy was used to observe the ultrastructural changes of skeletal muscle autophagosomes. Western blot was used to detect the expressions of Beclin1 and LC3II / I protein. Immunofluorescence was used to observe the localization and content of LC3.

RESULTS

The number of soleus muscle autophagosomes in group E was increased at 0, 12 and 24 hours after exercise, and LC3 autophagic fluorescence was significantly increased (<0.01), while autophagic fluorescence at 48 hours after exercise was still increased significantly (<0.05). Beclin1 and LC3II / I expression levels were increased after high-load centrifugal intervention (<0.05), and were peaked at 12 h~24 h after exercise (<0.01), and fully recovered at 72 h after exercise.

CONCLUSION

High-load eccentric exercise can induce ultrastructural changes in skeletal muscle autophagy and increase the expression of autophagy protein. The peak value appears at 12 hours after exercise. The above may be one of the reasons for the decline in skeletal muscle function caused by sports injury.

摘要

目的

探讨高负荷离心运动对大鼠自噬超微结构及自噬相关蛋白Beclin1和LC3II/I的影响。

方法

48只SD雄性大鼠经适应性训练后随机分为对照组(C组,n = 8)和高负荷离心运动组(E组,n = 40)。E组在跑台上进行90分钟下坡跑,于运动后0、12、24、48和72小时采集比目鱼肌。采用透射电子显微镜观察骨骼肌自噬体的超微结构变化。采用蛋白质免疫印迹法检测Beclin1和LC3II/I蛋白的表达。采用免疫荧光法观察LC3的定位及含量。

结果

E组比目鱼肌自噬体数量在运动后0、12和24小时增加,LC3自噬荧光显著增强(P<0.01),运动后48小时自噬荧光仍显著增加(P<0.05)。高负荷离心干预后Beclin1和LC3II/I表达水平升高(P<0.05),并在运动后12~24小时达到峰值(P<0.01),运动后72小时完全恢复。

结论

高负荷离心运动可诱导骨骼肌自噬超微结构改变,增加自噬蛋白表达,峰值出现在运动后12小时。上述情况可能是运动损伤导致骨骼肌功能下降的原因之一。

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