氯美昔布诱导肺癌细胞凋亡的作用机制

目的: 探讨氯美昔布诱导肺癌细胞凋亡的可能作用机制。方法: 人肺癌细胞株A549和NCI-H460 细胞先加入终浓度IL-1β₁ 1μg/L刺激 24 h,再加入不同浓度氯美昔布继续培养 24 h,采用Western blot 法检测ERK2、p-ERK及Bcl-2表达水平。氯美昔布体外处理A549、NCI-H460后,采用Western blot法检测Bcl-2、Bax表达水平。结果: 氯美昔布作用后肺癌细胞中ERK2及p-ERK的磷酸化水平均下降,并伴有Bcl-2水平的下降,差异有统计学意义(P<0.01)。并且随着氯美昔布浓度的增大, Bcl-2蛋白表达量逐渐下降,而Bax蛋白表达在A549细胞中增强,在NCI-H460细胞中不变,Bcl-2/Bax的比值下降。结论: 氯美昔布诱导肺癌细胞凋亡的机制可能与通过ERK信号转导途径调节肺癌细胞产生Bcl-2,进而诱导Bcl-2/Bax的比值下降有关。

Mechanisms of lumiracoxib on apoptosis in human lung cancer cells

AIM: To investigate the possible mechanism of Lumiracoxib (LUM)on the apoptosis of lung cancer cells.METHODS: Cells growing to confluence were treated with IL-1β (1 μg/L) prior to stimulation with LUM(0,15,30,60 μmol/L)for 24 hours. Western blot analysis was used to examine the level of ERK2, p-ERK and Bcl-2 protein in human NSCLC cell lines. Western blot analysis was used to examine the expression of Bcl-2 and Bax in A549 and NCI-H460 cells after exposed to various concentrations of LUM.RESULTS: LUM inhibited the up-regulated ERK2 and p-ERK as well as the down-regulated Bcl-2 expression in A549 and NCI-H460 cells. Additionally, LUM decreased the expression of Bcl-2 protein. And it increased the expression of Bax in A549 cells dependently on its doses. However, it had no effect on NCI-H460 cells. The ratio of Bcl-2/Bax decreased correspondingly.CONCLUSION: The mechanisms of the apoptotic effect of Lumiracoxib may be related to regulating Bcl-2 via ERK signal transduction pathway in human NSCLC cell lines.