论文部分内容阅读
目的探讨人参皂甙Rg3(ginsenoside Rg3,GS-Rg3)诱导人子宫内膜癌Ishikawa细胞株凋亡的作用及其信号通路。方法 Ishikawa细胞分为实验组和对照组。采用MTT法观察GS-Rg3对Ishikawa细胞生长的抑制作用,Transwell小室分析细胞体外的侵袭力,流式细胞术观察GS-Rg3对Ishikawa细胞周期的影响,Western blotting检测Caspase-3、P65蛋白的表达。结果经GS-Rg3作用后,Ishikawa细胞的生长受到明显的抑制(P<0.05),细胞侵袭力降低,S期细胞数增加,G2/M期细胞数减少(P<0.05),凋亡细胞数增加。Western blot检测显示,GS-Rg3作用Ishikawa细胞48h后,随着GS-Rg3浓度的增加,Caspase-3蛋白表达增加,P65蛋白表达下调,各实验组与对照组间比较有显著性差异(P<0.05)。结论 GS-Rg3可以通过下调P65蛋白的表达阻断NF-кB信号途径,抑制人子宫内膜癌Ishikawa细胞增殖,促进其凋亡。
Objective To investigate the effect of ginsenoside Rg3 (GS-Rg3) on apoptosis of human Ishikawa cell line and its signal pathway. Methods Ishikawa cells were divided into experimental group and control group. The inhibitory effect of GS-Rg3 on the growth of Ishikawa cells was observed by MTT assay. The invasiveness of cells in vitro was evaluated by Transwell assay. The effect of GS-Rg3 on the cell cycle of Ishikawa cells was observed by flow cytometry. The expressions of Caspase-3 and P65 protein were detected by Western blotting . Results After treated with GS-Rg3, the growth of Ishikawa cells was significantly inhibited (P <0.05), the invasiveness of cells decreased, the number of S phase cells increased, the number of G2 / M phase cells decreased (P <0.05) increase. Western blot analysis showed that after treated with GS-Rg3 for 48h, the expression of Caspase-3 increased and the expression of P65 decreased with the increase of GS-Rg3 concentration. There was significant difference between experimental group and control group (P < 0.05). Conclusion GS-Rg3 can down-regulate the expression of P65 protein and block the NF-кB signaling pathway, inhibit the proliferation and promote the apoptosis of Ishikawa cells.