Inhibitory effect of genistein on tert-butyl hydroperoxide-induced apoptosis of human vascular endothelial cells

王凡; 张婷; 糜漫天

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Inhibitory effect of genistein on tert-butyl hydroperoxide-induced apoptosis of human vascular endothelial cells

更新时间：2026-01-09

- Inhibitory effect of genistein on tert-butyl hydroperoxide-induced apoptosis of human vascular endothelial cells
- Journal of Army Medical University Vol. 32, Issue 23, Pages: 2507-2510(2010)
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  CLC： R151.3;R322.12;R329.28
- Published：2010
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王凡,张婷,糜漫天.染料木黄酮对叔丁基过氧化氢诱导的内皮细胞凋亡的抑制作用[J].陆军军医大学学报(原第三军医大学学报),2010,32(23):2507-2510.

　Wang Fan,Zhang Ting,Mi Mantian.Inhibitory effect of genistein on tert-butyl hydroperoxide-induced apoptosis of human vascular endothelial cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(23):2507-2510.
王凡,张婷,糜漫天.染料木黄酮对叔丁基过氧化氢诱导的内皮细胞凋亡的抑制作用[J].陆军军医大学学报(原第三军医大学学报),2010,32(23):2507-2510. DOI：

　Wang Fan,Zhang Ting,Mi Mantian.Inhibitory effect of genistein on tert-butyl hydroperoxide-induced apoptosis of human vascular endothelial cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(23):2507-2510. DOI：

摘要

目的研究染料木黄酮（genistein

Gen）对叔丁基过氧化氢（tert-butyl hydroperoxide，t-BHP）诱导的人血管内皮细胞株EA.hy926凋亡的保护效应并探索其相关分子机制。方法以t-BHP建立氧化应激损伤体外模型，设立空白对照组、Gen和t-BHP处理组，CCK-8法、流式细胞仪检测Gen对内皮细胞活力、凋亡的影响；Western blot法检测Gen对内皮细胞Caspase-3表达和PPARγ蛋白表达的影响；免疫细胞化学法检测Gen对细胞PPARγ表达定位。结果 t-BHP能明显抑制EA.hy926生长，至最大浓度240 μmol/L时，抑制率达到（93.66±4.66）%，与对照组相比，差异有统计学意义（P0.05），半数抑制浓度（IC50）约为100 μmol/L；Gen（5～5 000 nmol/L）能显著抑制t-BHP诱导的内皮细胞凋亡，并呈明显的剂量效应关系，500 nmol/L预处理组总凋亡率为（12.20±1.28）%，与对照组相比，差异有统计学意义（P0.05）；Gen能够显著激活PPARγ蛋白的表达，并诱导其核易位。结论 Gen对t-BHP诱导的内皮细胞凋亡有保护效应，其保护效应可能与PPARγ的活化有关。

Abstract

Objective To study the protective effect of genistein (Gen) on tert-butyl hydroperoxide (t-BHP)-induced apoptosis of human vascular endothelial cells (EA.hy926 cells) and its mechanism. Methods An in vitro model of t-BHP-induced oxidative stress injury was established. The cells were divided into control group

Gen treatment group and t-BHP treatment group. Effect of Gen on viability and apoptosis of EA.hy926 cells was detected by CCK-8 assay and flow cytometry

respectively. Effect of Gen on expression of Caspase-3 and peroxisome proliferators-activated receptor gamma (PPARγ) in EA.hy926 cells was detected by Western blotting. Results t-BHP significantly inhibited the apoptosis of EA.hy926 cells at the concentration of 240 μmol/L with an inhibitory rate of (93.66±4.66)% (P0.05). The IC50 was about 100 μmol/L. Gen at the concentration of 5 to 5 000 nmol/L significantly suppressed the t-BHP-induced apoptosis of EA.hy926 cells in a dose-dependent manner. The total apoptosis rate of EA.hy926 cells was (12.20±1.28）% when the concentration of t-BHP was 500 nmol/L (P0.05). Gen effectively activated the expression of PPARγ and induced translocation of its protein. Conclusion Gen has the protective effect on t-BHP-induced apoptosis of EA.hy926 cells possibly by activating PPARγ.

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