| Summary: | The gut microbial metabolite trimethylamine N-oxide (TMAO) has received increased attention due to its close relationship with cardiovascular disease and type 2 diabetes. In previous studies, TMAO has shown both harmful and beneficial effects on various tissues, but the underlying molecular mechanisms remain to be clarified. Here, we explored the effects of TMAO treatment on H<sub>2</sub>O<sub>2</sub>-impaired C2C12 myoblasts, analyzed metabolic changes and identified significantly altered metabolic pathways through nuclear magnetic resonance-based (NMR-based) metabolomic profiling. The results exhibit that TMAO treatment partly alleviated the H<sub>2</sub>O<sub>2</sub>-induced oxidative stress damage of cells and protected C2C12 myoblasts by improving cell viability, increasing cellular total superoxide dismutase capacity, improving the protein expression of catalase, and reducing the level of malondialdehyde. We further showed that H<sub>2</sub>O<sub>2</sub> treatment decreased levels of branched-chain amino acids (isoleucine, leucine and valine) and several amino acids including alanine, glycine, threonine, phenylalanine and histidine, and increased the level of phosphocholine related to cell membrane structure, while the TMAO treatment partially reversed the changing trends of these metabolite levels by improving the integrity of the cell membranes. This study indicates that the TMAO treatment may be a promising strategy to alleviate oxidative stress damage in skeletal muscle.
|
|---|