Microsorum membranaceum (D. Don) Ching protected dexamethasone-induced sarcopenia by targeting protein degradation and synthesis pathway in C2C12 cells and C57BL/6 mice

Microsorum membranaceum (D. Don) Ching have a great potential for improving sarcopenia as a form of muscle atrophy because its high antioxidant activity and traditional ailments improving effects.

This study aimed to investigate the protective effects and underlying mechanisms of a methanol extract of Microsorum membranaceum (MEM) against dexamethasone-induced sarcopenia.

After analyzing the ingredients and antioxidant properties of MEM, its effects on protein degradation and synthesis pathways, and muscle function were evaluated in dexamethasone (Dex)-treated C2C12 cells and C57BL/6 mice.

Fifteen components with bioactivity were detected using HPLC and high scavenging activities against free radicals were measured in MEM. In the protein degradation pathway, MEM suppressed the relative levels of ROS, MuRF1, and Atrogin-1 dose-dependently. In addition, MEM dose-dependently suppressed the expression level of LC3B and Beclin-1 in Dex + MEM-treated C2C12 cells. In the protein synthesis pathway, the MEM treatment induced the enhancement of PI3K, Akt and mTOR phosphorylation as well as the decrease of Myogenin and MyoD transcription in C2C12 cells with Dex-induced sarcopenia. These effects of MEM were well reflected by the increased myotube diameter in the Dex + MEM-treated C2C12 cells. The anti-sarcopenia effects of MEM were successfully verified in Dex-induced sarcopenia of the C57BL/6 mice. Furthermore, Dex + MEM-treated C57BL/6 mice showed significant recovery effects on the weight and function of muscle, as well as the section area of the calf muscle.

These results indicate that MEM can help prevent Dex-induced sarcopenia of C57BL/6 mice by targeting the protein degradation and synthesis pathways.