Muscle atrophy occurs in various physio-pathological conditions, including severe muscle injury, disuse, hormone imbalances, cancer, sepsis, and aging. A common feature of these conditions is the presence of cellular oxidative damage and pro-inflammatory processes. Dexamethasone (DEXA) is a synthetic glucocorticoid that is widely used as an anti-inflammatory agent. However, chronic DEXA treatment can lead to side effects such as diabetes mellitus, obesity, and, ultimately, muscle atrophy.

There is ongoing research aimed at identifying tools to counteract muscle atrophy and improve the quality of life of affected individuals. Among the promising approaches, the use of plant-based extracts has garnered significant attention. In particular, Moringa oleifera leaf extracts (MOLE) have been shown to support muscle cells metabolism and mitigate the negative effects of oxidative stress.

In this study, we investigated the effects of MOLE on DEXA-induced muscle atrophy and the underlying mechanisms in C2C12 myotubes.

Exposure to 100 mM DEXA for 24 hours induced muscle atrophy, as evidenced by increased levels of the specific markers such as MuRF-1 and Atrogin-1 and reduced levels of myosin heavy chain (MHC).

MOLE (0.15 mg/mg dried powder) was administered either concomitantly or 24 hours before or after DEXA exposure.

MOLE treatment was effective in reducing atrophy markers and improving the status of C2C12 myotubes, as reflected by increased MHC levels and fiber size in all experimental conditions involving DEXA.

Interestingly, the most pronounced effects were obtained when MOLE was administered to cells that had already undergone DEXA treatment.

In conclusion, these findings suggest that MOLE can alleviate DEXA-induced muscle atrophy in C2C12 myotubes by reducing atrophic markers and restoring the proper myotube phenotype.