摘要
目的:观察大黄素(emodin)对多药耐药白血病细胞株K562/Adr凋亡的影响及Akt-Caspase 3信号通路在其中的作用。方法:采用Annexin V/PI双染的流式细胞术和DNA倍体分析法检测细胞凋亡;Western blot法检测大黄素作用后不同时间段caspase-3前体蛋白、PARA、Akt、p-Akt表达水平的变化。结果:大黄素能够诱导K562/Adr细胞凋亡,并呈量效关系。大黄素作用K562/Adr细胞后caspase-3前体蛋白、Akt、p-Akt、PARA 116 KD表达水平下调,PARP 85 KD表达水平增加,并呈时效关系。结论:Akt-Caspase 3信号通路可能参与大黄素诱导K562/Adr细胞凋亡的过程。
Objective:To investigate the apoptosis-inducing effects of emodin on multidrug resistant leukemia cell line K562/Adr,and to explore the role of Akt-Caspase 3 signal pathway in apoptosis of K562/Adr cells treated with emodin.Methods:K562/Adr cells were exposed to emodin of different doses.The ability of emodin to induce apoptosis of K562/Adr cells was detected by Annexin V/PI double labeled flow cytometry and DNA ploidy analysis,the expressions of procaspase-3,PARP,Akt,p-Akt protein were determined by Western blot.Results:Apoptosis in K562/Adr cells could be induced by emodin in a dose dependent manner,Western blot results showed that emodin down-regulated the expression levels of procaspase-3,Akt,p-Akt,PARA 116 KD in treated K562/Adr cells,up-regulated expressions leves of PARP 85 KD in a time-dependent manner.Conclusion:The Akt-Caspase 3 signal pathway may be involved in these processes.
出处
《中国实验血液学杂志》
CAS
CSCD
北大核心
2015年第6期1556-1559,共4页
Journal of Experimental Hematology
基金
国家高技术研究发展计划-863计划(项目号:2012AA02A505)
卫生行业科研专项项目(项目号:201202017)
