染料木黄酮对人血管内皮细胞氧化应激损伤的保护作用

Protective effect of genistein on oxidative stress-induced injuries of human vascular endothelial cells

目的观察染料木黄酮(genistein,Gen)对人血管内皮细胞株EAhy.926氧化应激损伤保护效应并探讨其机制。方法用H2O2建立氧化应激损伤模型,CCK-8法检测Gen对细胞活力的影响;流式细胞仪和TUNEL法检测Gen对氧化应激诱导细胞凋亡的影响;Western blot检测Gen对Bcl-2、Nrf2、HO-1表达的影响。结果 H2O2明显影响细胞活力和诱导凋亡(IC50为650μmol/L),Gen(100～500 nmol/L)处理能显著抑制细胞活力下降,且细胞凋亡率由16.54%下降为6.18%;Gen对Bcl-2有上调作用;Gen能激活Nrf2/HO-1抗氧化途径。结论 Gen抑制血管内皮细胞的氧化应激损伤与对Bcl-2的调节和Nrf2/HO-1抗氧化途径的激活有关。

Objective To study the effect of genistein（Gen） on oxidative stress-induced injuries of human vascular endothelial cell line EA hy.926 and its mechanism.Methods Oxidative stress-induced injury model was established with H2O2.Effect of Gen on viability of cells and oxidative stress-induced apoptosis of cells was detected by CCK-8 assay,flow cytometry and TUNEL assay,respectively.Effect of Gen on expression of Bcl-2,Nrf2 and HO-1 was detected by Western blotting.Results H2O2 at the concentration of 100 to 500 nmol/L significantly inhibited the viability and apoptosis of cells（IC50=650 μmol/L）,with the apoptosis rate decreased from 16.54% to 6.18%.Gen up-regulated the expression of Bcl-2 protein and activated the anti-oxidation pathway of Nrf2 and HO-1.Conclusion Gen effectively inhibit oxidative stress-induced injuries of vascular endothelial cells by up-regulating the expression of Bcl-2 and activating the anti-oxidation pathway of Nrf2/HO-1.