Resveratrol protects human lens epithelial cells against H2O2-induced oxidative stress by increasing catalase, SOD-1, and HO-1 expression

摘要

Purpose: Oxidative damage induced by H2O2treatment can irreversibly damage the lens epithelium, resulting incell death and cataract. Whether the effects of oxidative stress couldbe attenuated in cultured human lens epithelial cells by incubationwith resveratrol (RES) is still unknown. In the present study, weexamined the function of resveratrol in protecting human lensepithelial B-3 (HLEB-3) cells against H2O2induced cell death and cell apoptosis, its role in reducing H2O2induced intracellular reactive oxygen species (ROS) accumulation, andinvestigated the mechanism by which resveratrol underlies the effect. Methods: HLEB-3 cells, a human lensepithelial cell line, were exposed to 100 μM H2O2with or without RES pre-treatment at different concentrations fordifferent time duration. Cell viabilities were monitored by4-[3-[4-iodophenyl]-2-4(4-nitrophenyl)-2H-5-tetrazolio-1,3-benzenedisulfonate](WST-1) assay. The apoptosis rate and ROS generation were detected byflow cytometric analysis. Expression levels of superoxide dismutases-1(SOD-1), catalase, and heme oxygenase-1 (HO-1) proteins were measuredby western-blotting analysis. p38 and c-jun N terminal kinase (JNK)activation was also evaluated by western-blotting analysis. Results: Resveratrol clearly reduced H2O2induced cell apoptosis and ROS accumulation; protected HLEB-3 cellsfrom H2O2 induced oxidative damage, and increasedthe expression levels of SOD-1, catalase, and HO-1. Further studiesshowed that RES also inhibited H2O2 induced p38and JNK phosphorylation. Conclusions: These findings suggestedthat RES protected HLEB-3 cells from H2O2 inducedoxidative damage, presumably by inducing three antioxidative enzymesincluding catalase, SOD-1, and HO-1.