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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。
Objective: To observe the effect of shikonin on the proliferation and apoptosis induction of HepG2 cells. Methods: HepG2 cells were treated with different concentrations of shikonin, the inhibitory effect of shikonin on the proliferation of HepG2 cells was detected by MTT, the activity of Caspase-3 was determined by colorimetric assay, and the expression of phosphorylated Akt protein (pAkt) was detected by Western blot . Results: Shikonin inhibited the proliferation of HepG2 cells in a concentration-and time-dependent manner. The shikonin-HepG2 cells showed a significant increase in Caspase-3 activity at 24 hours The time prolongs and increases; At the same time, shikonin treatment of HepG2 cells, with the increase of drug concentration, phosphorylated Akt protein expression decreased. Conclusion: Shikonin can inhibit the proliferation of HepG2 cells and induce the apoptosis of HepG2 cells. The mechanism of shikonin may be related to the inhibition of PI3K / Akt signaling by shikonin.