Propionibacterium freudenreichii MJ2 Improves Dexamethasone-Induced Muscle Atrophy in Rats by Increasing Muscle Mass...

Area of Science:

• Microbiology
• Cell Biology
• Physiology

Background:

• Muscle atrophy is the loss of muscle tissue due to various factors like aging, disease, and medication.
• Propionibacterium freudenreichii MJ2 (MJ2) exhibits anti-inflammatory and anti-obesity effects.
• Dexamethasone (DEX) is a corticosteroid known to induce muscle atrophy.

Purpose of the Study:

• To investigate the effects of MJ2 on dexamethasone (DEX)-induced muscle atrophy in vitro (C2C12 myoblasts) and in vivo (rats).

Main Methods:

• C2C12 myoblasts and rats were treated with DEX to induce muscle atrophy.
• MJ2 (live and heat-killed HK-MJ2) was administered to assess its protective effects.
• Key molecular markers for muscle atrophy, apoptosis, and protein synthesis were analyzed.
• Muscle strength, mass, and fiber area were measured in rats.

Main Results:

• HK-MJ2 prevented the reduction in myotube diameter caused by DEX in C2C12 cells.
• MJ2 downregulated atrophy-related genes (MuRF-1, Atrogin-1) and apoptosis markers (Bax/Bcl-2) while upregulating muscle synthesis proteins (p-Akt/Akt, p-mTOR/mTOR) in DEX-treated cells.
• Both live and HK-MJ2 significantly improved grip strength, muscle mass, and muscle fiber area in rats with DEX-induced muscle atrophy.

Conclusions:

• Live and heat-killed MJ2 demonstrate efficacy in mitigating DEX-induced muscle atrophy.
• MJ2 treatment promotes muscle mass and fiber area preservation, offering a potential therapeutic strategy for muscle wasting.