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秦皮乙素通过调控Smac、Survivin蛋白对SGC-7901细胞凋亡机制的研究 被引量:4

Mechanism by Which Aesculetin Induces Apaptosis of SGC-7901 Cells Through Regulating the Smac、Survivin Protein
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摘要 目的:研究秦皮乙素对活性氧、膜电位、Ca^(2+)以及Smac、Survivin蛋白活性的影响,为进一步揭示其抗肿瘤作用机制提供帮助。方法:MTT法检测对肿瘤细胞生长的抑制作用;流式细胞仪检测细胞内活性氧、Ca^(2+)以及膜电位变化情况;westenblot法测定对Surviving、Smac蛋白含量的影响。结果:秦皮乙素可显著提高SGC-7901细胞生长抑制率,升高活性氧和细胞内Ca^(2+)浓度,降低线粒体膜电位,增加Smac蛋白含量,降低Surviving蛋白含量,与对照组比较具有统计学意义。结论:秦皮乙素可通过调控活性氧和细胞内Ca^(2+)浓度,以及线粒体膜电位来启动线粒体凋亡通路,进而释放Smac蛋白,并与凋亡抑制蛋白Surviving蛋白结合,从而发挥其抗肿瘤作用。 Objective : The experiment based on Aesculetin of ROS, Ca2+,membrane potential and its influence to the Smac, Sur- vivin protein activity, further research on the anti-tumor mechanism, for the research of Aesculetin, anti-tumor mechanism to provide theoretical added. Method: By determined by MTT method to detect growth inhibition rate, Flow cytometry instrument to detect intra- cellular reactive oxygen species and Ca2 + concentration as well as the membrane potential changes, Westen blot method surviving, smac protein content. Result:Aesculetin can enhance the cells growth inhibition rate of SGC-7901 cells, Increased reactive oxygen concentration and Ca2+ concentration, Reduce: the mitochondrial membrane potential, Increased the smac protein content and Reduces the surviving protein content. Conclusion: Aesculetin can regulate active oxygen concentration and Ca2+ concentration, and mitochon- drial membrane potential to start the mitochondrial apeptotic pathways, Releasing the smac protein to Combin with apeptosis inhibiting protein surviving protein, so as to fulfill its antitumor effect.
出处 《黑龙江医药》 CAS 2016年第1期21-24,共4页 Heilongjiang Medicine journal
基金 哈尔滨商业大学博士科研启动项目(14LG01)
关键词 秦皮乙素 SGC-7901 细胞凋亡 抗肿瘤 Aesculetin SGC-7901 Cell apoptosis Antitumor
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