ERK1/2在黄芪多糖促进HepG2细胞凋亡中的作用

The Role of ERK1/2 in Astragalus Polysaccharide-induced Apoptosis in HepG2 Cell Line

目的:阐明黄芪多糖与ERK1/2通路在HepG2细胞凋亡中的作用。方法:实验分为4组:空白对照组(control);B组,20 mg.L-1黄芪多糖3个剂量处理组(AP,20,40,80 mg.L-1黄芪多糖处理组(AP,40,80 mg.L-1),药物处理24 h后检测各指标。应用Western blot,MTT,TUNEL,线粒体膜电势检测等方法检测黄芪多糖对HepG2细胞生存凋亡及细胞中ERK1/2表达量的影响。结果:MTT与TUNEL表明黄芪多糖对HepG2细胞的凋亡具有促进作用,增加HepG2细胞的caspase-3的活性,降低(HepG2)细胞线粒体的膜电位,降低Bcl-2表达;黄芪多糖可以降低ERK1/2的表达,表明黄芪多糖的凋亡促进作用可能通过ERK1/2途径。结论:黄芪多糖可以通过抑制ERK1/2信号通路促进HepG2细胞的凋亡。

Objective：Although astragalus polysaccharide（AP） is known to have apoptotic effect in many cancer cells,the mechanisms are still poorly understood.We aim to test whether apoptotic effect of astragalus polysaccharide is regulated by the ERK1/2 pathway in HepG2 cells.Method： Cells were divided into 4 groups and treated with different pharmaceuticals：control,group 20,40,80 mg·L-1AP.We studied the effect of AP on cell survival using Western blot,cell viability measurement,TUNEL assay and mitochondrial potential analysis,caspase-3 activity measurement.Result： Astragalus polysaccharide has apoptotic responses in HepG2 cells,including mitochondrial depolarization and the apoptosis-specific proteins up-regulation,Bcl-2 down-regulation.Conclusion： These results suggest that ERK1/2 pathway is necessary for the effects of astragalus polysaccharide in inhibiting cell proliferation of HepG2 cells.