Human hepatocytes were treated with a selenium-enriched peptide from Cardamine violifolia (SPE) to study whether SPE could interfere with ethanol-induced hepatocyte injury. An oxidative stress model was constructed via the alcohol-induced injury of THLE-2 hepatocytes. After treatment with SPE at different concentrations of organic selenium, the cell injury and oxidative stress related indicators were measured to evaluate the cell protection and antioxidant capacity. The results showed that the concentration of ethanol of 1 000 mmol/L and the action time of ethanol of 12 h led to significant damage of THLE-2 cells (P<0.05). SPE treatment significantly increased the cell viability (P<0.05), which reached 78.02% at selenium concentration of 12 μmol/L. Compared with the injury group, the contents of aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase in the supernatant of SPE treatment group was significantly reduced (P<0.05). Moreover, after SPE treatment, the content of reactive oxygen species in THLE-2 cells was decreased, and the levels of superoxide dismutase, glutathione peroxidase, catalase, and glutathione were significantly increased (P<0.05), with the highest values of 34.68 U/mg, 974.75 nmol/g, 1.76 U/mg, and 55.58 μmol/g, respectively; among them, glutathione peroxidase was highly expressed, at about 5.6 times that of the injury group, probably because SPE provided selenium ions for glutathione peroxidase synthesis. In addition, the apoptosis rate was decreased, and the mitochondrial membrane potential was increased in the SPE treatment group. Above all, the selenium-enriched polypeptide of Cardamine violifolia alleviated alcoholic liver injury by regulating oxidative stress related indicators.
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