Establishment of a dexamethasone-induced zebrafish skeletal muscle atrophy model and exploration of its mechanisms

• Published in: Experimental gerontology 2024-12, Vol.198, p.112615, Article 112615
• Main Authors: Sun, Chen-Chen, Li, Ye-Jun, Zhu, Dan-Ting, Chen, Zhang-Lin, Xiao, Jiang-Ling, Chen, Xiang-Tao, Zheng, Lan, Peng, Xi-Yang, Tang, Chang-Fa
• Format: Article
• Language: English
• Subjects: Animals; Autophagy - drug effects; Dexamethasone; Dexamethasone - pharmacology; Disease Models, Animal; Endoplasmic reticulum stress; Endoplasmic Reticulum Stress - drug effects; Glucocorticoids - pharmacology; Mitochondrial dysfunction; Muscle, Skeletal - drug effects; Muscle, Skeletal - pathology; Muscular Atrophy - chemically induced; Muscular Atrophy - pathology; Skeletal muscle atrophy; Swimming; Zebrafish
• ISSN: 0531-5565; 1873-6815; 1873-6815
• DOI: 10.1016/j.exger.2024.112615

Skeletal muscle atrophy is one of the main side effects of high-dose or continuous use of glucocorticoids (such as dexamethasone). However, there are limited studies on dexamethasone-induced skeletal muscle atrophy in zebrafish and even fewer explorations of the underlying molecular mechanisms. This study aimed to construct a model of dexamethasone-induced skeletal muscle atrophy in zebrafish and to investigate the molecular mechanisms. Zebrafish soaked in 0.01 % dexamethasone solution for 10 days. Loli Track (Denmark) and Loligo Swimming Respirometer were used to observe the effect of dexamethasone on swimming ability. The effects of dexamethasone on zebrafish skeletal muscle were observed by Transmission electron microscopy, H&E, and wheat germ agglutinin techniques. Enriched genes and signaling pathways were analyzed using Transcriptome sequencing. Further, the levels of mitochondrial and endoplasmic reticulum-related proteins were examined to investigate possible mechanisms. 0.01 % dexamethasone reduced zebrafish skeletal muscle mass (p