Loquat Leaf Extract Inhibits Oxidative Stress-Induced DNA Damage and Apoptosis via AMPK and Nrf2/HO-1 Signaling Pathways in C2C12 Cells

Loquat (Eriobotrya japonica) leaf extract exhibits bioactive properties against a variety of diseases. However, it remains unclear whether loquat leaf extract can protect myoblasts from oxidative damage. To investigate the protective effect of loquat leaf ethanol extract (LE) against hydrogen peroxide (H2O2)-induced oxidative stress in C2C12 murine myoblasts and the effect of LE on cellular differentiation in C2C12 cells. LE inhibited H2O2-induced cytotoxicity and reduced both the expression level of γ-H2AX and reactive oxygen species formation. LE also inhibited H2O2-induced apoptosis, which resulted in the upregulation of B-cell lymphoma 2 and pro-caspase-3 and inhibition of poly(ADP-ribose) polymerase cleavage, and the dysfunction of mitochondria under H2O2-induced oxidative stress, which inhibited the release of cytochrome c from mitochondria to the cytoplasm. Moreover, LE upregulated p-AMP-activated protein kinase (AMPK), p-nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) and downregulated Kelch-like ECH-associated protein 1 in H2O2-treated C2C12 cells. In addition, LE promoted the differentiation of C2C12 cells into myotubes and increased the expression levels of myogenic proteins, myogenic differentiation 1 (MyoD) and myogenin. These findings suggest that LE may be a promising therapeutic candidate for treating oxidative stress-mediated myoblast injury and enhancing cellular differentiation of C2C12 murine myoblasts into myotubes.