青藤碱诱导肺癌 NCI-H460 细胞凋亡及其机制的实验研究

摘要

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 Bel -2 and a increase of Bax expression. SIN combined with the inhibitors of PI3K/Akt and MAPK/ERK pathways 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 Bel - 2 and Bax; combined SIN and the inhibitors of PDK/Akt and MAPK/ERK pathways may be synergistically induced apoptosis of lung cancer cells,it may provide new drug for treatment of lung cancer.%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PBK/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PI3 K/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.