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人参皂苷CK对胃癌细胞株SGC-7901及其内源性VEGF的影响[J]. 肿瘤防治研究, 2011, 38(01): 17-20. DOI: 10.3971/j.issn.1000-8578.2011.01.005
引用本文: 人参皂苷CK对胃癌细胞株SGC-7901及其内源性VEGF的影响[J]. 肿瘤防治研究, 2011, 38(01): 17-20. DOI: 10.3971/j.issn.1000-8578.2011.01.005
Effects of Ginsenoside CK on Gastric Cancer SGC-7901 Cell Line and Endogenous VEGF Secreted by Tumor Cells[J]. Cancer Research on Prevention and Treatment, 2011, 38(01): 17-20. DOI: 10.3971/j.issn.1000-8578.2011.01.005
Citation: Effects of Ginsenoside CK on Gastric Cancer SGC-7901 Cell Line and Endogenous VEGF Secreted by Tumor Cells[J]. Cancer Research on Prevention and Treatment, 2011, 38(01): 17-20. DOI: 10.3971/j.issn.1000-8578.2011.01.005

人参皂苷CK对胃癌细胞株SGC-7901及其内源性VEGF的影响

Effects of Ginsenoside CK on Gastric Cancer SGC-7901 Cell Line and Endogenous VEGF Secreted by Tumor Cells

  • 摘要: 目的 研究人参皂苷CK对胃癌SGC-7901细胞增殖、细胞周期的影响及其对内源性分泌的血管内皮细胞生长因子(VEGF)的作用。方法 以50、25、12.5、6.25、3.125、1.5625μg/ml的人参皂苷CK作用于胃癌细胞株SGC-7901,通过MTT法检测人参皂苷CK对细胞的抑制作用;采用流式细胞术检测细胞周期和细胞凋亡;ELISA定量检测细胞培养液中内源性VEGF的含量变化。结果 MTT法显示人参皂苷CK对胃癌细胞株SGC-7901有抑制作用,并且呈浓度、时间依赖关系;SGC-7901细胞经人参皂苷作用后出现明显凋亡峰,且细胞周期被阻滞在G0/G1期;人参皂苷CK处理组VEGF含量低于对照组(P<0.05),高浓度组低于低浓度组(P<0.05),且随着作用时间延长,VEGF含量降低。结论 人参皂苷CK可通过诱导凋亡抑制胃癌细胞株SGC-7901生长,并可抑制SGC-7901细胞内源性分泌VEGF,人参皂苷CK可能成为一种潜在的抗胃癌药物。

     

    Abstract: Abstract:Objective To investigate the effects of Ginsenoside CK on the cell proliferation、cell cycle and endogenous VEGF of gastric cancer SGC-7901 cell line. Methods SGC-7901 cell line in cultural medium in vitro were given 50,25,12.5,6.25,3.125,1.5625 μg/ml Ginsenosde CK. The inhibitory rate of cell line was measured by MTT assay; cell apoptotic rate and cell phase were detected by flow Cytometry (FCM); the VEGF contents were detected by ELISA assay. Results It was found that Ginsenoside CK had significant inhibitory effect on the proliferation of SGC-7901 cell line,and this effect was dose-and-time-dependent; FCM assay indicated that apoptosis peak appeared evidently after the cells being interfered with Ginsenoside CK and most of cells were arrested in G0/G1 phase; The levels of VEGF in Ginsenoside CK groups were lower than that in the control group (P<0.05). The level of VEGF in the groups of high concentration Ginsenoside CK were lower than that in the group of low concentration(P<0.05), and the VEGF contents decrease with action time prolonging. Conclusion Ginsenoside CK dramatically inhibits proliferation of SGC-7901 cell line by inducing cell apoptosis and secretion of endogenous VEGF. Ginsenoside CK may become a potential drug in the prevention and treatment of gastric cancer.

     

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