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目的:探讨杨梅树皮素(myricetin,MYR)对人肝癌HepG-2抑制生长和诱导凋亡作用及其机制。方法:MTT法研究MYR对人肝癌HepG-2的抑制生长;荧光染色和电子透射电镜观察HepG-2细胞形态;流式细胞仪研究MYR对HepG-2细胞周期的影响及诱导凋亡作用,罗丹明123单染观察MYR对线粒体膜电位的改变;caspase 3,9试剂盒检测MYR对人肝癌HepG-2细胞内caspase3,9活性的影响。结果:MYR对人肝癌HepG-2细胞生长具有明显的抑制作用,并具有剂量依赖性,IC50为58.6617 mg.L-1;MYR作用72 h后,HepG-2细胞呈现典型细胞凋亡特征,细胞周期阻滞于G2/M期,凋亡率最高为64.73%。同时线粒体膜电位明显下降,caspase3,9活性增加。结论:MYR对人肝癌HepG-2细胞有明显的抑制生长和诱导凋亡作用,其机制可能与线粒体凋亡途径有关。
Objective: To investigate the effect of myricetin (MYR) on the growth inhibition and apoptosis induced by HepG-2 and its mechanism. METHODS: The inhibitory effect of MYR on HepG-2 cells was studied by MTT assay. The morphology of HepG-2 cells was observed by fluorescence staining and electron transmission electron microscopy. The effect of MYR on the cell cycle of HepG-2 cells was observed by flow cytometry. The effect of MYR on the activity of caspase 3 and 9 in human hepatocellular carcinoma HepG-2 cells was examined by caspase 3,9 kit. Results: MYR significantly inhibited the growth of HepG-2 cells in a dose-dependent manner with an IC50 of 58.6617 mg.L-1. After treated with MYR for 72 h, HepG-2 cells showed typical characteristics of apoptosis, Cycle arrest in G2 / M phase, the highest rate of apoptosis was 64.73%. At the same time mitochondrial membrane potential decreased significantly, caspase3,9 activity increased. Conclusion: MYR can significantly inhibit the growth and induce apoptosis of HepG-2 human hepatoma cells, which may be related to the mitochondrial apoptotic pathway.