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付鹏宇,胡扬,李燕春,于加倍,朱镕鑫,贾杰,龚丽景.低氧暴露所致大鼠骨骼肌萎缩的蛋白转化调节机制[J].中国实验动物学报,2019,27(4):423~432.
低氧暴露所致大鼠骨骼肌萎缩的蛋白转化调节机制
Protein turnover regulation mechanism of rat skeletal muscle atrophy induced by hypoxia
投稿时间:2019-03-01  
DOI:10. 3969 / j.issn.1005-4847. 2019. 04. 002
中文关键词:  低氧暴露  骨骼肌萎缩  半饥饿状态  骨骼肌蛋白转化调节  肌肉类型  大鼠
英文关键词:hypoxic exposure  skeletal muscle atrophy  semi-starvation state  protein turnover-regulatory pathways  muscle types  rat
基金项目:
作者单位E-mail
付鹏宇 北京体育大学运动人体科学学院,北京 100084 1402884452@ qq.com 
胡扬 北京体育大学中国运动与健康研究院,北京 100084  
李燕春 北京体育大学中国运动与健康研究院,北京 100084  
于加倍 北京体育大学运动人体科学学院,北京 100084  
朱镕鑫 1. 北京体育大学运动人体科学学院,北京 100084
2. 上海体育科学研究所,上海 200030 
 
贾杰 北京体育大学运动人体科学学院,北京 100084  
龚丽景 北京体育大学中国运动与健康研究院,北京 100084 lijing.gong@bsu.edu.cn 
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中文摘要:
      目的 对比低氧暴露和常氧下配对低氧摄食干预(半饥饿状态)下大鼠骨骼肌蛋白质合成和分解相关基因表达的差异,以探讨低氧暴露诱导骨骼肌萎缩发生的可能机制。方法 SD 大鼠分为:①常氧正常饮食组(C组);②低氧正常饮食组(H 组),氧气浓度为12. 4%;③常氧配对饮食组(P 组),投食量即为H 组前一天摄食量。4周干预后测量大鼠体成分,取比目鱼肌(SOL)和趾长伸肌(EDL),称量湿重;HE 染色观察肌纤维形态,计算肌纤维横截面积(FCSA);WB 测试骨骼肌中HIF1α、Akt、p-Akt 及骨骼肌蛋白合成和分解相关基因蛋白含量。结果 1)H组大鼠体重较C 组持续下降,P 组与C 组间无显著性差异;干预初期H 组(P 组同)摄食量较C 组显著下降,后期两组间无差异;(2)干预后,H 组大鼠体质量和肌肉总量较C 组和P 组显著性降低,P 组与C 组间无差异;H 组两肌肉湿重较C 组显著下降;H 组EDL 的FCSA 显著低于C 组和P 组;(3)H 组EDL 中HIF1α 蛋白含量显著高于C 组;H组和P 组SOL 中p-Akt/ Akt 比值显著低于C 组;H 组EDL 中mTOR、4EBP1 蛋白含量显著低于C 组,atrogin 1、MuRF1、beclin 1 蛋白含量及LC3Ⅱ/ Ⅰ比值显著高于C 组,H 组SOL 中MuRF1 蛋白含量显著高于C 组和P 组。结论 低氧所致的骨骼肌萎缩由低氧特异性因素诱发,表现为以快肌为主的骨骼肌蛋白合成减少和分解增加,而非低氧下摄食量减少引起。
英文摘要:
      Objective The aim of this study was to identify the mechanism underlying skeletal muscle atrophyinduced by hypoxia exposure. To this aim, expression levels of different types of skeletal muscle protein synthesis- anddegradation-related genes were compared between rats that had experienced hypoxic exposure and normoxia in a hypoxicfeeding intervention (semi-starvation state). Methods SD rats were divided into a normoxic normal diet group (groupC), a hypoxic normal diet group (group H; oxygen concentration of 12. 4%), or a normoxia-matched diet group (group P;the food intake was matched to that of group H). The body composition of rats was tested by DEXA after the 4-weekintervention. The soleus (SOL) and the extensor digitorum longus (EDL) muscles were collected and weighed. Musclesfiber histology was observed using HE staining, and the muscle fiber cross-sectional area (FCSA) was calculated. Theprotein contents of HIF1α, Akt, p-Akt, and skeletal muscle protein synthesis- and degradation-related genes were detectedusing Western blot. Results  1) Body weight was lower in the group H than group C, but there was no significantdifference between the groups P and C during the intervention period. At the beginning of the intervention, the food intakeof group H (which was the same as group P) was significantly lower than that of the group C, and there was no significantdifference between the two groups. (2) After the intervention, the body weight and muscle mass were significantly lower inthe group H compared to groups C and P; the wet weights of SOL and EDL muscles in the group H were significantly lowerthan those of the group C; and the FCSA of the EDL muscle was significantly lower in the group H than in groups C and P.(3) HIF1α protein contents of the EDL muscle was significantly higher in the group H than group C; the ratio of p-Akt/Akt of the SOL muscle in the groups H and P was significantly lower than that of the group C; mTOR and 4EBP1 proteinlevels in the EDL muscle of group H was significantly lower than group C; atrogin1, MuRF1, and Beclin1 protein levelsand the ratio of LC3II/ I in EDL of the group H were significantly higher than those of the group C, and MuRF1 proteinlevel in the SOL muscle of group H was significantly higher than that of the groups C and P. Conclusions Skeletal muscleatrophy caused by hypoxia is induced by hypoxia-specific factors, showing that decreased synthesis and decomposition ofskeletal muscle proteins, which is manifested by a decrease in skeletal muscle protein synthesis and a decrease in decomposition of fast muscle fibers, rather than a decrease in food intake under hypoxia.
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