Effects of photobiomodulation on the differentiation, viability, and migration of C2C12 myoblasts exposed to different concentrations of dexamethasone

Abstract Glucocorticoid-induced muscle atrophy remains a clinical concern because of its broad impact on skeletal muscle structure, metabolism, and regenerative capacity. This study examined whether photobiomodulation (PBM) could lessen the damaging effects of dexamethasone (DEXA) on C2C12 myoblasts during differentiation. Cells were exposed to 5, 10, or 200 µM DEXA and evaluated after 24, 48, and 72 h. A single PBM session was delivered using a 780-nm laser (70 mW, 1.05 J, 26.25 J/cm 2 ). Cell viability and proliferation were assessed by MTT and crystal violet assays; differentiation was analyzed through nuclear fusion and morphological staining; migration was measured using the wound-healing assay; and IL-6 and TNF-α levels were quantified by ELISA. DEXA reduced C2C12 viability, fusion, and migration in a time- and dose-dependent manner, particularly at 10 and 200 µM. PBM alone was not cytotoxic and, when combined with DEXA, partially preserved viability, enhanced proliferation, and supported early differentiation, although without restoring control levels. Migration was also mitigated, but not fully recovered. PBM further moderated the DEXA-induced reduction in IL-6 and TNF-α. Overall, PBM mitigated the effects of glucocorticoid-induced stress, indicating its potential as a complementary approach to help preserve myogenic function.