Effect of Photobiomodulation on C2C12 Myoblasts Cultivated in M1 Macrophage‐conditioned Media

Moderate levels of a proinflammatory macrophages phenotype are indispensable and play an important role in the skeletal muscle repair process since this response depends on their secreted products concentration to influence and modulate muscle inflammation as well as the differentiation of myoblasts. This study investigated the effects of photobiomodulation (PBM) on undifferentiated and differentiation‐induced C2C12 myoblasts cultivated in different concentrations of M1 phenotype macrophage‐conditioned media of J774 cells (MCM1) also submitted to PBM using the same irradiation parameters. Irradiation was performed once with low‐level laser (780 nm, 70 mW, 1 J) and was evaluated cell viability, proliferation and differentiation, nitric oxide (NO) synthesis and IL‐6 and TNF‐α protein levels 24 and 48 h after C2C12 irradiation. PBM treatment in undifferentiated myoblasts exhibited lower IL‐6 levels in the presence of nonirradiated MCM1 at both concentrations. Myoblasts in proliferation condition cultivated with irradiated MCM1 showed lower IL‐6 and TNF‐α levels after 48 h in the presence of both concentrations evaluated. PBM induced a decrease in the synthesis of NO on undifferentiated and differentiation‐induced myoblasts. PBM was able to reduce the level of proinflammatory protein and markers, which are important to allow the differentiation of myoblasts during the muscle repair process. The muscle repair is dependent on moderate levels of mediators secreted from macrophages. This study investigated the effects of photobiomodulation (PBM: 780 nm) on undifferentiated and differentiation‐induced C2C12 myoblasts cultivated in an activated M1 macrophage‐conditioned medium submitted to irradiation with the same parameters. Results showed that the increase synthesis of proinflammatory markers could inhibit the fusion of myoblasts. PBM was able to modulate the viability and proliferation of myoblasts and promoted reductions in nitric oxide, IL‐6 and TNF‐α synthesis.