Abstract:To investigate the protect effects of thyroid hormone(T3) on HepG2 with oxidative damage. Establishing an oxidative stress model of HepG2 cells cultured in vitro, adding different concentrations of T3 for protection, determining the differentiation of cellular ROS, survival, antioxidant enzymes and related genes. Pretreatment of 10-9, 10-7, 10-5 mol/L T3 for 24 h, the level of ROS significantly reduced and the survival rate of cells was significantly increased(p<0.05)in cells of 50, 100, 200 μmol/L H2O2 processing respectively. While, 10-5 mol/L T3 increased the level of ROS. The amount of T3 can significantly reduce MDA content(p<0.05), increase T-AOC, GSH-Px and SOD activity of cells of H2O2 oxidative damage(p<0.05). But excess T3 increased MDA content and decreased the antioxidant activity. The results of gene expression showed that T3 pretreatment significantly increased PI3K, Nrf2 in the damaged cells(p<0.05). T3 can improve the redox state of HepG2 cells of H2O2 oxidative damage because of the effect on antioxidant enzyme activities and the expression of anti-oxidation genes and the effect is related to the dose and cell damage levels.
