PESV干预K562细胞PI3K/Akt信号通路凋亡调控的研究  

Study on PI3K/Akt messenger passage and apoptosis controlling in PESV-preconditioned K562 cells

作　　者：张蕾[1] 杨文华[1] 于文俊[2] 郝征[2] 张佳[2] 

机构地区：[1]天津中医药大学第一附属医院,天津300193 [2]天津中医药大学,天津300193

出　　处：《天津中医药》2012年第3期274-277,共4页Tianjin Journal of Traditional Chinese Medicine

基　　金：教育部博士点基金项目(20091210110004)

摘　　要：[目的]探讨PESV对K562细胞PI3K/Akt信号蛋白及凋亡调控因子Bcl-2和Bad表达的影响。[方法]将体外培养K562细胞,经PESV处理不同时间后,流式细胞术检测细胞凋亡率,Western blot检测PI3K及p-Akt蛋白水平变化,实时荧光定量RT-PCR检测Bcl-2、Bad mRNA水平变化。[结果]与对照组相比,PESV处理后K562细胞凋亡率显著增加,PI3K及p-Akt表达降低,抗凋亡相关基因Bcl-2 mRNA表达降低,促凋亡基因Bad mRNA表达增加。[结论]PESV可能通过降低PI3K、Akt信号蛋白表达,调节Bcl-2和Bad表达,抑制K562细胞增殖,促进其凋亡。[Objective] To investigate the effect of PESV on the expression of massage protein PI3K / Akt,apoptosis regulators Bcl-2 and Bad expression in K562 cells.[Methods] In vitro cultured K562 cells preconditioned with PESV for different times were determined for cell apoptosis rate with cytoflowmeter,the level of PI3K and p-AKT protein with Western blot and Bcl-2,Bad mRNA level by realtime fluorescence quantitative RT-PCR.[Results] Compared with the control group,the apoptosis rate of PESV treated K562 cells was significantly increaseds,the expression of PI3K and p-Akt and anti-apoptosis-related gene Bcl-2 mRNA was decreased;the expression of pro-apoptotic gene Bad mRNA was increased.[Conclusion] PESV may regulate the expression of Bcl-2 and Bad,inhibit the proliferation of K562 cells and promote their apoptosis by reducing the expression of PI3K and Akt signaling protein.

关 键 词：PESV K562细胞系 凋亡 PI3K Akt Bcl-2 BAD 

分 类 号：R733.72[医药卫生—肿瘤]