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

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.