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目的:探讨细胞周期蛋白依赖激酶(CDK)抑制剂Roscovitine(Ros)诱导非小细胞肺癌(NSCLC)A549细胞凋亡及其作用机制。方法:以不同浓度Ros(10μM、20μM、40μM)处理细胞24h,采用Annexin V-PI染色以流式细胞仪检测细胞凋亡,Westernblot法检测胞浆中和线粒体促凋亡蛋白Bax和Bad的表达,流式细胞仪检测线粒体膜电位(MMP)变化。结果:Ros以剂量依赖的方式诱导A549细胞凋亡,同时Bad和Bax在胞浆的含量随着Ros剂量的增加而减少,而在线粒体中却出现相反的结果,线粒体膜电位随Ros剂量的增大而降低。结论:Ros可通过促进Bax和Bad由胞浆向线粒体易位,诱导NSCLC A549细胞由线粒体途径发生凋亡。
AIM: To investigate the apoptosis induced by Roscovitine (Ros), a cell cycle inhibitor of protein kinase (CDK), and its mechanism in A549 cells. Methods: The cells were treated with different concentrations of Ros (10μM, 20μM, 40μM) for 24 hours. Cell apoptosis was detected by flow cytometry with Annexin V-PI staining. The expressions of Bax and Bad in cytoplasm and mitochondria were detected by Western blot , Flow cytometry mitochondrial membrane potential (MMP) changes. Results: Ros could induce the apoptosis of A549 cells in a dose-dependent manner. At the same time, the content of Bad and Bax in the cytoplasm decreased with the increase of Ros dosage, but the opposite result appeared in mitochondria. The mitochondrial membrane potential increased with the increase of Ros dosage Big and lower. Conclusion: Ros can induce mitochondrial apoptosis in NSCLC A549 cells by promoting the translocation of Bax and Bad from cytoplasm to mitochondria.