Bovine collagen oligopeptides mitigate dexamethasone-induced muscle atrophy via PI3K/Akt/mTOR signaling pathway in mice model and C2C12 cell

Sarcopenia, the age-related decline in muscle mass and strength, is a major health issue that impairs life quality and increases risks of adverse health effects. Nutrition is vital for muscle health. Bovine collagen oligopeptides (BCOP) are proven to reduce muscle soreness and fatigue. However, little is currently known about the effects of BCOP on muscle atrophy. The present study was designed to evaluate the mitigating effects of BCOP on dexamethasone-induced muscle atrophy mice model and C2C12 myoblasts in vitro and in vivo. BCOP supplementation in mice increased lean mass, improved grip strength, and modulated serum nutrition and inflammation. It also restored muscle structure and reduced atrophy markers. In C2C12 cells, BCOP enhanced myotube growth and downregulated atrophy markers. The PI3K/Akt/mTOR signaling pathway was activated by BCOP intervention both in mice model and C2C12 myotube. These findings suggest that BCOP may serve as a potential therapeutic agent for sarcopenia. • In the present study, we evaluated the effect of BCOP on dexamethasone-induced muscle atrophy in vivo and in vitro. The results are comprehensive and credible. • BCOP improves serum nutritional markers and reduces inflammation in mice. • Our study reveals that BCOP activates PI3K/Akt/mTOR pathway, potentially via downregulating MuRF1 and MAFbx, key in muscle protein balance.