Muscle atrophy refers to the loss or wasting of muscle tissue caused by medication, aging, disease, and injury. Propionibacterium freudenreichii MJ2 (MJ2) shows anti-inflammatory and anti-obesity properties. This study aimed to determine the effects of MJ2 on dexamethasone (DEX)-induced muscle atrophy in C2C12 myoblast cell line and rats. Heat-killed P. freudenreichii MJ2 (HK-MJ2) inhibited a decrease in the diameter of DEX-treated C2C12 myotubes. Additionally, it downregulated the expression of muscle atrophy- and apoptosis-related genes (MuRF-1, Atrogin-1, and Bax/Bcl-2) in DEX-treated C2C12 cells while activating proteins (p-Akt/Akt and p-mTOR/mTOR) associated with muscle protein synthesis. Live- and HK-MJ2 treatment increased grip strength, muscle mass, and muscle fiber area in rats with DEX-induced muscle atrophy. In conclusion, both live- and HK-MJ2 increase muscle mass and muscle fiber area, resulting in the improvement of DEX-induced muscle atrophy.
Kim et al. (Sun,) studied this question.