紫草素对人肝癌HepG2细胞增殖的抑制及诱导凋亡作用

目的:观察紫草素抑制人肝癌HepG2细胞增殖及凋亡诱导的作用。方法:用不同浓度的紫草素处理HepG2细胞,MTT检测紫草素对HepG2细胞生长增殖的抑制作用;比色法测定Caspase-3酶活性;Western blot法检测磷酸化Akt蛋白(pAkt)的表达。结果:紫草素能够抑制人肝癌HepG2细胞的增殖,并呈浓度、时间依赖性,紫草素与HepG2细胞作用24小时后Caspase-3酶活性显著增强,显示紫草素诱导的调亡作用随时间的延长而增加;同时,紫草素处理HepG2细胞后,随着药物浓度的增加,磷酸化Akt蛋白表达下降。结论:紫草素可抑制人肝癌细胞HepG2的增殖,诱导HepG2细胞凋亡,凋亡机制可能与紫草素抑制PI3K/Akt信号途径有关。

Effects of Proliferation Inhibition and Apoptosis Induction of Shikonin on HepG2 Cells

Objective:To investigate the inhibitory effects of shikonin on proliferation inhibition and apoptosis induction in human hepatoma HepG2 cells and its possible mechanism.Methods:The proliferation inhibition was measured by MTT assay.Colorimetric method was employed to detect the activity of caspase-3.The expression of phosphorylation Akt(pAkt) was measured by Western blotting assay.Results:Shikonin inhibited HepG2 cells growth in a time and dose-dependent manner.After treatment with Shikonin for 24 hours, the activity levels of caspase-3 significant increased, but the expression of pAkt was markedly decreased.Conclusions:Shikonin can inhibit the growth and induce the apoptosis of HepG2 cells significantly, which may be related with the PI3/Akt signal pathway.