吲哚-3-原醇对人肺癌细胞株A549的促凋亡和增殖抑制作用  

Effect of indole-3-carbinol on proliferation and apoptosis of A549 cells

作　　者：付娟[1,2] 尹宜发 姚霞[1,2] 杨欣[1,2] 

机构地区：[1]三峡大学第二人民医院 [2]宜昌市第二人民医院,湖北宜昌443000

出　　处：《实用药物与临床》2015年第7期761-764,共4页Practical Pharmacy and Clinical Remedies

基　　金：国家自然科学基金(81100264)

摘　　要：目的探讨吲哚-3-原醇(Indol-3-carbinol,I3C)对肺腺癌细胞株A549细胞增殖和凋亡的影响及其作用机制。方法将对数生长期的A549细胞分别用不同浓度的I3C处理(0、25、50、100μg/m L)。细胞培养72 h后,采用M TT观察I3C对A549细胞的增殖抑制作用;Annexin V-PI/FITC检测细胞凋亡;Western blotting检测细胞中PI3K、p-AKT、Bax、Bcl-2、Cleavage-PARP、Clevage-Caspase3蛋白的变化。结果 I3C可以呈浓度依赖性地诱导A549细胞的增殖抑制和凋亡,上调Bax和Cleavage-PARP、Cleavage-Caspase3表达,下调PI3K、p-AKT和Bcl-2,对AKT表达无明显影响。结论 I3C可通过抑制PI3K/AKT信号通路而诱导A549细胞增殖抑制和凋亡。Objective To investigate the effect and mechanisms of the indole-3-carbinol on the apoptosis and proliferation of human lung adenocarcinoma cells line A549. Methods The A549 cells at logarithmic grow th phase w ere divided into control group and I3 C groups. The cells w ere normally treated w ith different concentrations of I3C（ 0,25,50,100 μg /m L）. MTT and Annexin V-PI/FITC were used to examine the proliferation and apoptotic changes of the A549 cell after incubation for 72 h,respectively. The changes of PI3 K,p-AKT,AKT,Bax,Bcl-2,Cleavage-PARP and Cleavage-Caspase3 protein w ere detected by Western blotting. Results The results show ed that I3 C treatment can decrease the proliferation of A549 and the expression of PI3 K,p-AKT and Bcl-2 and increase the apoptosis rate of A549,the expression of Cleavage-PARP,Cleavage-Caspase3 and Bax. Moreover,I3 C had no influence on the expression of AKT. Conclusion I3 C can induce the apoptosis and grow th inhibition of human lung adenocarcinoma cells line A549 and the mechanism is involved in PI3 K / AKT signaling.

关 键 词：吲哚-3-原醇 A549 增殖 凋亡 PI3K/AKT 

分 类 号：R734.2[医药卫生—肿瘤]