Abstract: Objective: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·L^-1 EGF+OGD group,10 μg·L^-1 EGF+ OGD group and 20 μg·L^-1 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 Bcl-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·L^-1 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·L^-1 EGF 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·L^-1 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.

Key words: deep tissue injury, reactive oxygen species, epithelial growth factor, skeletal muscle L6 cells, mitochondria, oxygen-glucose deprivation