Abstract
This study aimed to investigate the regulatory functions of Sijunzi decoction on mitochondrial dysfunction in muscle atrophy progression. Cell viability was assessed using Cell Counting Kit-8 assay, and protein expressions were investigated using Western blot. The adenosine triphosphate level was measured using an adenosine triphosphate commercial kit, and the oxygen consumption rate was evaluated using the MitoXpress® Xtra oxygen consumption assay kit. Tetramethylrhodamine staining was used to quantify mitochondrial membrane potential, and C2C12 cells were treated with dexamethasone (1 μM) for 48 h to create a muscle atrophy model. We found that the decreased cell viability stimulated by dexamethasone treatment was reversed after Sijunzi treatment (50 μg/mL and 100 μg/mL). Additionally, Sijunzi treatment suppressed dexamethasone-stimulated C2C12 myotube atrophy and ameliorated dexamethasone-triggered mitochondrial dysfunction. Sijunzi treatment retarded the adenosine 5’-monophosphate-activated protein kinase/forkhead box O3 pathway. We demonstrated that Sijunzi regulates AMPK/FOXO3a-mediated mitochondrial dysfunction and alleviates DEX-induced C2C12 myotube muscle atrophy.
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