摘要
目的:探讨丹参酮ⅡA抑制非小细胞肺癌NCI-H520细胞生长及其分子机制。方法:用不同浓度的丹参酮ⅡA(0,5,10,20μM)处理非小细胞肺癌NCI-H520细胞后,采用MTT法检测非小细胞肺癌NCI-H520细胞活力;采用流式细胞计检测非小细胞肺癌NCI-H520细胞周期;应用免疫印迹方法检测蛋白表达水平。结果:丹参酮ⅡA显著抑制非小细胞肺癌NCI-H520细胞生长,并呈浓度依赖方式;流式细胞检测到丹参酮ⅡA处理非小细胞肺癌NCI-H520细胞后,细胞周期S期细胞比例较处理前显著增多(P<0.05);免疫印迹实验检测到丹参酮ⅡA处理非小细胞肺癌NCI-H520细胞后,细胞周期蛋白Cyclin E及CDK2抑制剂P27较处理前显著上调(P<0.05)。结论:丹参酮ⅡA可能通过上调P27抑制CDK2,导致非小细胞肺癌细胞NCI-H520细胞周期S阻滞。
Objective： To explore the molecular mechanism by which Tanshinone Ⅱ A （Tan Ⅱ A） inhibits non-small cell lung cancer NCI-H520 cells. Method： After dealing with different concentrations of Tanshinone Ⅱ A （0, 5, 10, 20μM）, the viability of NCI-H520 cells treated with Tanshinone Ⅱ A was detected by MTF as- say ： Cell cycle profile of NCI-H520 cells induced by Tanshinone Ⅱ A was examined by Flow Cytometry ： Immunob- lotting was utilized to determine proteins expression level. Result： Tanshinone Ⅱ A remarkably detriments NCI- H520 cells viability in dose-dependent manner： cell cycle analysis indicated the proportion of NCI-H520 cells in cell cycle S-phase increased after treatment of Tanshinone Ⅱ A. Further, Immunoblotting showed the upregulation of cyclin E and CDK inhibitor i〉27, in NCI-H520 cells treated with Tanshinone Ⅱ A. Conclusion： Tanshinone Ⅱ A arrested NCI-H520 cell cycle at S arrest maybe by the upregulation of F27 which inhibits CDK2.
出处
《新医学》
2013年第5期347-350,共4页
Journal of New Medicine
基金
广东省医学科研基金(B2012171)
