Preclinical research demonstrates that MJ2 treatment increases muscle mass and reduces muscle atrophy in rats, indicating therapeutic potential for muscle wasting conditions.
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.
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Kim et al. (2026) studied this question.
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