染料木黄酮对人血管内皮细胞氧化应激损伤的保护作用

张婷; 王凡; 朱俊东; 易龙; 付钰洁; 糜漫天

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染料木黄酮对人血管内皮细胞氧化应激损伤的保护作用

论著 | 更新时间：2026-01-09

- 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
- 陆军军医大学学报 2011年33卷第3期页码：229-232
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  中图分类号： R282.71;R322.12;R363.27
- 纸质出版：2011
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张婷,王凡,朱俊东,易龙,付钰洁,糜漫天.染料木黄酮对人血管内皮细胞氧化应激损伤的保护作用[J].陆军军医大学学报(原第三军医大学学报),2011,33(03):229-232.

　Zhang Ting,Wang Fan,Zhu Jundong,Yi Long,Fu Yujie,Mi Mantian.Protective effect of genistein on oxidative stress-induced injuries of human vascular endothelial cells[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(03):229-232.
张婷,王凡,朱俊东,易龙,付钰洁,糜漫天.染料木黄酮对人血管内皮细胞氧化应激损伤的保护作用[J].陆军军医大学学报(原第三军医大学学报),2011,33(03):229-232. DOI：

　Zhang Ting,Wang Fan,Zhu Jundong,Yi Long,Fu Yujie,Mi Mantian.Protective effect of genistein on oxidative stress-induced injuries of human vascular endothelial cells[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(03):229-232. DOI：

摘要

目的观察染料木黄酮（genistein

Gen）对人血管内皮细胞株EA hy.926氧化应激损伤保护效应并探讨其机制。方法用H

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 H

明显影响细胞活力和诱导凋亡（IC

为650 μmol/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。

Abstract

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 H

. 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 H

at the concentration of 100 to 500 nmol/L significantly inhibited the viability and apoptosis of cells

(IC

=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.

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