白藜芦醇通过影响线粒体膜电位诱导HepG2细胞凋亡

目的 研究白藜芦醇诱导HepG2细胞凋亡的机制，探讨白藜芦醇诱导HepG2细胞凋亡过程中线粒体膜电位的变化。方法采用MTT法测定白藜芦醇对HepG2细胞的生长抑制作用，通过荧光染色及流式细胞术检测细胞凋亡，电子显微镜观察细胞超微结构的变化，用Rhodaminel23和TMRE标记细胞线粒体膜电位（△ψ），并分别通过流式细胞仪和共聚焦激光扫描显微镜检测。结果低浓度白藜芦醇（≤25μmoFL）对HepG2细胞的生长抑制作用不显著，而高浓度白藜芦醇（〉25μmol／L）显著地抑制HepG2细胞的生长，且呈时间和浓度的依赖性（F=18．532，P〈0．05）；流式细胞术分析显示，白藜芦醇能显著诱导HepG2细胞凋亡，且呈浓度依赖性（P〈0．05）；白藜芦醇能降低HepG2细胞线粒体膜电位。结论白藜芦醇抑制HepG2细胞增殖，并诱导细胞凋亡，白藜芦醇使HepG2细胞线粒体膜电位去极化，提示线粒体膜电位去极化在白藜芦醇诱导细胞凋亡的过程中起作用。

Resveratrol induces HepG2 cell apoptosis by depolarizing mitochondrial membrane

Objective To investigate the effects of resveratrol on the proliferation, apoptosis, mitochondrial membrane potential and cell morphology of human liver cancer cell line HepG2. Methods The changes in HepG2 cell growth and proliferation in response to resveratrol treatment were evaluated by MTT assay, and resveratrol-induced apoptosis of HepG2 cells was investigated by flow cytometry. Inverted microscope and electron microscope were employed for observing morphological changes of the treated cells. The whole-cell mitochondrial membrane potential was measured in separate experiments using two fluorimetric probes, rhodamine123 and TMRE, respectively. HepG2 cells treated with rhodamine123 were analyzed by flow cytometry and cells treated with TMRE by confocal microscope. Results MTT assay showed that low concentrations of resveratrol produced no significant effect on the growth of HepG2 cells, whereas at high concentrations, resveratrol could obviously inhibit the cell growth in a time- and dose-dependent manner. Resveratrol also induced apoptosis of HepG2 cells, and after a 24-hour treatment, resveratrol caused sharp increment of the mitochondria membrane potential. Conclusion Resveratrol is capable of inhibiting the proliferation of HepG2 cells and inducing cell apoptosis by depolarizing mitochondrial membrane potential.