Melatonin Attenuates H₂O₂-Induced Muscle Atrophy and Promotes Hypertrophy: Morphological, Redox, and Gene Evidence.
TL;DR
Melatonin demonstrated protective effects against HⁿOⁿ-induced muscle atrophy in C2C12 cells, particularly through the preservation of myotube morphology and enhancement of cellular antioxidant status.
Abstract
INTRODUCTION Disuse muscle atrophy is strongly associated with oxidative stress, with antioxidants such as melatonin emerging as potential therapeutic agents, particularly due to their protective effects on mitochondrial function. This study aimed to investigate the effects of melatonin on redox balance, cellular morphology, and expression of atrophy-related genes, Atrogin-1 and MuRF1, in an H2O2-induced muscle atrophy model using the C2C12 cell line.
Materials And Methods
Four experimental groups were established, namely Control, Melatonin, H2O2, and Melatonin + H2O2. Morphological alterations were evaluated by measuring myotube diameters. Redox status was assessed using the Oxidative Stress Index (OSI), calculated from Total Antioxidant Status (TAS) and Total Oxidant Status (TOS). The expression levels of Atrogin-1 and MuRF1 were analyzed using quantitative real-time PCR.
Results
Significant differences in myotube diameters were observed among the groups (p < 0.05). The Melatonin + H2O2 group exhibited the lowest OSI values, indicating improved redox balance. Although the differences were not statistically significant, melatonin treatment was associated with lower expression levels of Atrogin-1 and MuRF1 compared to other groups.
Discussion
The findings suggest that melatonin may alleviate oxidative stressinduced muscle atrophy by preserving myotube morphology and improving cellular redox balance. The observed trends in Atrogin-1 and MuRF1 expression indicate a potential modulatory effect of melatonin on atrophy-related pathways; however, additional time-course and protein-level analyses are needed to further clarify these mechanisms.
Conclusion
Melatonin demonstrated protective effects against HⁿOⁿ-induced muscle atrophy in C2C12 cells, particularly through the preservation of myotube morphology and enhancement of cellular antioxidant status. These findings support the potential role of melatonin as a therapeutic candidate for oxidative stress-related muscle atrophy.