Protective effect of epithelial growth factor on oxidative damage of skeletal muscle cells in model rats of oxygen-glucose deprivation / 吉林大学学报(医学版)

ABSTRACT

To set up the rat skeletal muscle L6 cell models of oxygen-glucose deprivation (OGD) in vitro, and to investigate the protective effect of EGF in deep tissue injury (DTI) of pressure sores. Methods: The rat skeletal muscle cells in the logarithmic phase were divided into normal control group, OGD group, 5 μg · L1 EGF+OGD group, 10 μg · L1 EGF+ OGD group and 20 μg · L1 EGF+ OGD group. The survival rates of skeletal muscle cells in various groups were measured by MTT assay; the cell apoptotic rates in various groups were detected by flow cytometry; the reactive oxygen species (ROS) levels were detected by DCFH-DA; Rhodamine 123 was used to detect the mitochondrial membrane potential; the expressions of Bax and Bel-2 proteins were determined by Western blotting method. Results: Compared with normal control group, the survival rates of skeletal muscle cells in OGD group after 24 h OGD was significantly decreased (P<0.05); the apoptotic rate was markedly increased (P<0.01); the ROS level was increased (P<0.01); the mitochondrial membrane potential was decreased (P<0.01); the ratio of Bcl-2/Bax was significantly decreased (P<0.01). Compared with OGD group, the survival rates of skeletal muscle cells in different concentrations of EGF groups were increased and the apoptotic rates were decreased, especially in 10 and 20 μg · L1 EGF groups (P<0.05 or P<0.01); the ROS levels in skeletal muscle cells in different concentrations of EGF groups were decreased and the mitochondrial membrane potential were increased, especially in 10 and 20 μg · L1EGF groups (P<0.05 or P<0.01); the Bcl-2/Bax ratios were significantly decreased in a concentration-dependent manner, especially in 10 and 20 μg · L1 EGF groups (P<0.05 or P<0.01). Conclusion: EGF can improve the skeletal muscle cell injury induced by OGD in a concentration-dependent manner via decreasing the ROS levels and protecting the cell mitochondrial function.