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

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 MO(2)max 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 sod1 and sod2, and the protein expression of Nox2 were significantly increased. In addition, we found that the inflammatory factors Il1 beta and Tnf alpha were significantly enriched in skeletal muscle, and the expression of the HMGB1/TLR4/NF-kappa B 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.

Automated summary

This study investigated the effect of alcohol on skeletal muscle using a zebrafish model and revealed its molecular mechanism. The results showed that alcohol exposure led to decreased body size, skeletal muscle fiber size, swimming performance, and oxygen consumption in zebrafish. Alcohol also increased the expression of markers for muscle atrophy and autophagy, as well as inflammation and oxidative stress.