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酒精通过HMGB1/TLR4/NF-κB信号通路诱导斑马鱼骨骼肌萎缩。

Alcohol Induces Zebrafish Skeletal Muscle Atrophy through HMGB1/TLR4/NF-κB Signaling.

作者信息

Wen Wei, Sun Chenchen, Chen Zhanglin, Yang Dong, Zhou Zuoqiong, Peng Xiyang, Tang Changfa

机构信息

Key Laboratory of Physical Fitness and Exercise Rehabilitation of Hunan Province, College of Physical Education, Hunan Normal University, Changsha 410012, China.

出版信息

Life (Basel). 2022 Aug 10;12(8):1211. doi: 10.3390/life12081211.

Abstract

Excessive alcohol consumption can cause alcoholic myopathy, but the molecular mechanism is still unclear. In this study, zebrafish were exposed to 0.5% alcohol for eight weeks to investigate the effect of alcohol on skeletal muscle and its molecular mechanism. The results showed that the body length, body weight, cross-sectional area of the skeletal muscle fibers, Ucrit, and MOmax of the zebrafish were significantly decreased after alcohol exposure. The expression of markers of skeletal muscle atrophy and autophagy was increased, and the expression of P62 was significantly reduced. The content of ROS, the mRNA expression of and , and the protein expression of Nox2 were significantly increased. In addition, we found that the inflammatory factors Il1β and Tnfα were significantly enriched in skeletal muscle, and the expression of the HMGB1/TLR4/NF-κB signaling axis was also significantly increased. In summary, in this study, we established a zebrafish model of alcohol-induced skeletal muscle atrophy and further elucidated its pathogenesis.

摘要

过量饮酒会导致酒精性肌病,但其分子机制仍不清楚。在本研究中,将斑马鱼暴露于0.5%的酒精中8周,以研究酒精对骨骼肌的影响及其分子机制。结果显示,酒精暴露后斑马鱼的体长、体重、骨骼肌纤维横截面积、临界游泳速度(Ucrit)和最大代谢率(MOmax)显著降低。骨骼肌萎缩和自噬标志物的表达增加,而P62的表达显著降低。活性氧(ROS)含量、[具体基因1]和[具体基因2]的mRNA表达以及Nox2的蛋白表达显著增加。此外,我们发现炎症因子Il1β和Tnfα在骨骼肌中显著富集,HMGB1/TLR4/NF-κB信号轴的表达也显著增加。总之,在本研究中,我们建立了酒精诱导的骨骼肌萎缩斑马鱼模型,并进一步阐明了其发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e628/9410481/7ea9eb97a71c/life-12-01211-g001.jpg

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