人参皂甙Rg3作用PI3K/AKT通路诱导人子宫内膜癌Hec-1-B细胞凋亡的研究

目的:探讨人参皂甙Rg3(ginsenoside Rg3,GS-Rg3)作用PI3K/AKT通路对Hec-1-B细胞的诱导凋亡作用。方法:采用MTT法观察GS-Rg3对Hec-1-B细胞生长的抑制作用;流式细胞术观察GS-Rg3作用Hec-1-B细胞后对Hec-1-B细胞凋亡的影响;Transwell小室分析细胞体外的侵袭力;Western blotting检测PI3K、AKT的表达。结果:GS-Rg3对Hec-1-B细胞的体外增殖有明显的抑制作用(P<0.05),并随着药物浓度和时间增加其抑制作用更加明显,在一定浓度范围内呈剂量、时间依赖性。GS-Rg3能够诱导Hec-1-B细胞凋亡,细胞端粒酶PI3K、AKT表达水平及活性显著降低。结论:GS-Rg3能够通过诱导人子宫内膜癌Hec-1-B细胞发生凋亡而发挥抑制细胞生长作用,抑制PI3K、AKT的活性是GS-Rg3体外诱导人子宫内膜癌Hec-1-B细胞发生凋亡的重要作用机制之一。

Study on the inducing effect of ginsenoside Rg3 on apoptosis of human endometrial cancer Hec-1-B cells by impacting PI3K/AKT pathway

Objective:To explore the inducing effect of ginsenoside Rg3(GS-Rg3) on apoptosis of human endometrial cancer Hec-1-B cells by impacting PI3K/AKT pathway.Methods:MTT method was used to observe the inhibiting effect of GS-Rg3 on proliferation of Hec-1-B cells;flow cytometry was used to observe the effect of GS-Rg3 on apoptosis of Hec-1-B cells;Transwell chamber mode was used to analyze the invasive ability of Hec-1-B cells in vitro;Western blotting was used to detect the expressions of PI3K and AKT.Results:GS-Rg3 inhibited the proliferation of Hec-1-B cells in vitro markedly(P<0.05),and the effect enhanced with the increase of drug concentration and time,showing a dose-and time-dependent manner within a certain concentration.GS-Rg3 induced apoptosis of Hec-1-B cells,the expression levels and activities of PI3K and AKT decreased significantly.Conclusion:GS-Rg3 has an inhibiting effect on the proliferation of human endometrial cancer Hec-1-B cells by inducing apoptosis of human endometrial cancer Hec-1-B cells,inhibiting the activities of PI3K and AKT is one of the important mechanisms of GS-Rg3 inducing apoptosis of Hec-1-B cells in vitro.