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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 observe the protective effect of Genistein on the oxidative stress injury of human vascular endothelial cell line EAhy.926 and to explore its mechanism. Methods H2O2 was used to establish the model of oxidative stress injury. The effect of Gen on cell viability was detected by CCK-8 assay. The effect of Gen on oxidative stress-induced apoptosis was detected by flow cytometry and TUNEL. The effect of Gen on Bcl-2 , Nrf2, HO-1 expression. Results H2O2 significantly affected cell viability and induced apoptosis (IC50 was 650μmol / L). Gen (100 ~ 500 nmol / L) treatment significantly inhibited cell viability and apoptosis rate from 16.54% to 6.18% Bcl-2 is up-regulated; Gen activates the Nrf2 / HO-1 antioxidant pathway. Conclusion Gen inhibited the oxidative stress injury of vascular endothelial cells in the regulation of Bcl-2 and the activation of Nrf2 / HO-1 antioxidant pathway.