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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。
AIM: To investigate the apoptosis-inducing effects of ginsenoside Rg3 (GS-Rg3) on Hec-1-B cells induced by PI3K / AKT pathway. Methods: The inhibitory effect of GS-Rg3 on Hec-1-B cell proliferation was observed by MTT assay. The effect of GS-Rg3 on Hec-1-B cell apoptosis was observed by flow cytometry. Transwell Cell invasion assay in vitro; Western blotting detection of PI3K, AKT expression. Results: GS-Rg3 significantly inhibited the proliferation of Hec-1-B cells in vitro (P <0.05). The inhibitory effect of GS-Rg3 on Hec-1-B cells was more pronounced with dose and time dependent Sex. GS-Rg3 can induce Hec-1-B cell apoptosis, the expression level and activity of telomerase PI3K, AKT were significantly decreased. Conclusion: GS-Rg3 can inhibit the growth of Hec-1-B cells by inducing the apoptosis of human endometrial carcinoma Hep-1-B cells. Inhibition of PI3K and AKT activity is an effect of GS- B cell apoptosis one of the important mechanisms of action.