Overexpression of Stanniocalcin 2 Protects Differentiated QM7 Cells from H2O2-Induced Oxidative Damage

Oxidative stress, caused by excessive reactive oxygen species (ROS) accumulation, is a major factor in muscle cell damage and muscle atrophy-related disorders. Although Stanniocalcin 2 (STC2) is involved in cellular stress and exhibits cytoprotective effects in various cell types, its role in skeletal muscle cells during oxidative stress is unclear. This study investigated the effects of STC2 overexpression in quail muscle (QM7) cells exposed to H2O2-induced oxidative stress. STC2 expression was upregulated in non-transfected QM7 cells following H2O2 treatment. Stable STC2-overexpressing cells were differentiated for 4 days, and then assessed for cell viability, ROS accumulation, cell death, and myotube morphology following H2O2 treatment. Compared with control cells, STC2-overexpressing cells exhibited higher cell viability, reduced ROS accumulation, and decreased cell death. STC2 overexpression also attenuated the H2O2-induced reduction in MyHC protein expression. Antioxidant-related genes, including Superoxide Dismutase 1, Glutathione Peroxidase 1, Heme Oxygenase 1, and NAD(P)H Quinone Dehydrogenase 1, were significantly upregulated in STC2-overexpressing cells. Compared with the control cells, nuclear factor erythroid 2-related factor 2 protein levels were not increased in STC2-overexpressing cells under oxidative stress conditions. These findings suggest that STC2 overexpression alleviates oxidative stress-induced cellular damage and may contribute to protective antioxidant responses in muscle cells.