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作 者:王宝庆[1] 李艳春[2] 泰文娇[2] 张为革[3] 马恩龙[2] 高文远[1]
机构地区:[1]天津大学药物科学与技术学院,天津300072 [2]沈阳药科大学生命科学与生物制药学院,辽宁沈阳110016 [3]沈阳药科大学制药工程学院,辽宁沈阳110016
出 处:《沈阳药科大学学报》2009年第1期52-54,58,共4页Journal of Shenyang Pharmaceutical University
摘 要:目的研究(±)2-(7,8,3′,4′,5′-五甲氧基)黄烷(PMF)体外对人胃癌SGC-7901细胞的增殖抑制作用及机制。方法MTT法检测不同浓度PMF体外对SGC-7901细胞的增殖抑制作用;流式细胞仪检测PMF对细胞周期分布的影响;Western blot法检测PMF对凋亡相关蛋白PARP、caspase-3表达的影响。结果不同浓度的PMF作用72 h可剂量依赖性地抑制SGC-7901细胞增殖;PMF作用12 h可使SGC-7901细胞周期阻滞于G2/M期;PMF作用24 h细胞周期检测可见亚二倍体峰(SubG1),并可诱导细胞凋亡相关蛋白PARP、caspase-3的活化。结论PMF体外可抑制人胃癌SGC-7901细胞的增殖,其增殖抑制作用与诱导G2/M周期阻滞和细胞凋亡有关。Objective To investigate the growth inhibitory effect and mechanism of (±)2-(7,8,3′,4′,5′- pentamethoxyflavan) (PMF) on human gastric cancer SGC-7901 cells. Methods SGC-7901 cells were treated with different concentration of PMF. The growth inhibition was measured by MTT assay; the change of cell cycle distribution was determined by flow cytometry analysis;the activation of PARP and caspase-3 was probed using Western blot assay. Results After treatment with PMF for 12 h,the growth of SGC-7901 cells were significantly inhibited in a dose-dependent manner;meanwhile, the cell cycle SGC-7901 was arrested at GJM phase. Moreover, the sub-G1 peak was detected by flow cytometry analysis, and the activation of PARP and caspase-3 was observed in SGC-7901 cells treated with PMF for 24 h. Conclusions PMF inhibits the growth of SGC-7901 cells through arrest of G2/M and induction of apoptosis.
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