青藤碱诱导肺癌NCI-H460细胞凋亡及其机制的实验研究  

Research of sinomenine-induced cell apoptosis and its mechanism in lung cancer cell NCI-H460

作　　者：栾虹[1] 周立平[1] 郑军[1] 王朔[1] 张青杨[1] 

机构地区：[1]中国医科大学附属第一医院检验科,辽宁沈阳110001

出　　处：《现代肿瘤医学》2012年第10期2004-2006,共3页Journal of Modern Oncology

基　　金：辽宁省教育厅科研计划项目(编号:L2010695)

摘　　要：目的:探究青藤碱(SIN)诱导肺癌NCI-H460细胞凋亡的作用机制。方法:四甲基偶氮唑蓝(MTT)法测定SIN对肺癌NCI-H460细胞生长的影响;Western blot测定Bcl-2,Bax蛋白的表达;用SIN、PI3K/Akt和MAPK/ERK信号通路抑制剂干预NCI-H460细胞,流式细胞术检测细胞的凋亡率。结果:SIN对肺癌NCI-H460细胞生长有抑制作用,呈时间、浓度依赖性;SIN可以使NCI-H460细胞Bcl-2表达减低,Bax增强;SIN与PI3K/Akt和MAPK/ERK信号通路抑制剂联用后可协同增加NCI-H460细胞凋亡(P<0.05)。结论:SIN可以抑制肺癌NCI-H460细胞的生长,能改变其Bax,Bcl-2蛋白的表达,与PI3K/Akt和MAPK/ERK信号通路抑制剂联用可协同发挥促进肺癌细胞凋亡作用,可望成为新的肺癌治疗药物。Objective：To explore the mechanism of sinomenine - induced NCI - H460 cell apoptosis. Methods： MTT was used to detect the growth of NCI - H460 cells, Bcl - 2 and Bax protein levels were assessed by Western blot analysis, sinomenine（SIN） and inhibitors of PI3K/Akt and MAPK/ERK were used to interfere NCI - H460 cells, then the apoptosis rate of cells was detected by flow cytometry. Results ： SIN inhibited the growth of NCI - H460 cells in a time -dependent and concentration -dependent manners. Meantime, SIN treatment led to a significant decrease of Bcl- 2 and a increase of Bax expression. SIN combined with the inhibitors of PI3K/Akt and MAPK/ERK path- ways could enhance the apoptosis rate of NCI - H460 cells （ P 〈 0.05 ）. Conclusion ： SIN could inhibit growth of NCI - H460 cells and change the expressions of Bcl - 2 and Bax; combined SIN and the inhibitors of PI3K/Akt and MAPK/ERK pathways may be synergistically induced apoptosis of lung cancer cells,it may provide new drug for treat- ment of lung cancer.

关 键 词：青藤碱 NCI-H460细胞 凋亡 

分 类 号：R733.7[医药卫生—肿瘤] R734.2[医药卫生—临床医学]