摘要
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 study the mechanism of myricetin inducing the HepG-2 cell line apoptosis.Method： The MTT method was employed to study myricetin pharmacodynamics in HepG-2.The light microscope and transmission was used to identify the tumor cell apoptosis in the morphology.The FCM method and the kit of caspase 3,caspase 9 were hired to detect the apoptosis rates,the content of mitochondrial membrane electric potential and the activity of caspase in cancer cells.Result： Myricetin significantly inhibits the proliferation and induces the apoptosis of HepG-2 in a dose-dependent manner,which is accompanied with G2/M and S phase arrest.In addition,myricetin also increases the activation of caspase 3,9 and results in a depolarization and ΔΨm collapse in a dose-dependent manner.Conclusion： The molecular pathway of apoptosis of human hepatocellular carcinoma cell lines induced by myricetin might deal with the mitochondria-mediated pathway.
出处
《中国中药杂志》
CAS
CSCD
北大核心
2010年第8期1046-1050,共5页
China Journal of Chinese Materia Medica
基金
黑龙江省教育厅骨干教师项目
