Propionibacterium freudenreichii MJ2 Improves Dexamethasone-Induced Muscle Atrophy in Rats by Increasing Muscle Mass and Muscle Fiber Area

TL;DR

This study shows that Propionibacterium freudenreichii MJ2 can help reduce muscle atrophy caused by dexamethasone in rats.

Contribution

The novel finding is that both live and heat-killed MJ2 improve muscle atrophy by increasing muscle mass and fiber area.

Findings

Heat-killed MJ2 inhibits the decrease in C2C12 myotube diameter caused by dexamethasone.

MJ2 treatment increases grip strength, muscle mass, and muscle fiber area in rats with DEX-induced atrophy.

MJ2 downregulates atrophy-related genes and activates muscle protein synthesis pathways.

Abstract

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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