氯美昔布诱导肺癌细胞凋亡的作用机制

中国临床药理学与治疗学 ›› 2012, Vol. 17 ›› Issue (1): 47-51.

氯美昔布诱导肺癌细胞凋亡的作用机制

郝吉庆¹, 孙耕耘², 沈玉先³

¹安徽医科大学第一附属医院肿瘤内科
²呼吸内科
³教育部重要遗传病基因资源利用重点实验室(省部共建), 合肥 230022,安徽

收稿日期:2011-10-25 修回日期:2011-12-15 出版日期:2012-01-26 发布日期:2012-02-16
作者简介:郝吉庆,女,博士,主任医师、副教授,硕士生导师,从事肿瘤内科治疗工作。Tel: 0551-2923615 E-mail: ayfy_hjq@163.com

Mechanisms of lumiracoxib on apoptosis in human lung cancer cells

HAO Ji-qing¹, SUN Gen-yun², SHEN Yu-xian³

¹Department of Oncology
²Department of Pulmonary Disease, the First Affilicated Hospital of Anhui Medical University, Hefei 230022,Anhui, China;
³Key Laboratory of Gene Resource Utilization for Genetic Diseases of Ministry of Education and Anhui Province, Hefei 230032, Anhui, China

Received:2011-10-25 Revised:2011-12-15 Online:2012-01-26 Published:2012-02-16

摘要/Abstract

摘要： 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。

关键词: 氯美昔布, 肺癌, 细胞凋亡, 机制

Abstract: 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.

Key words: Lumiracoxib, Lung cancer, Apoptosis, Mechanism

中图分类号:

郝吉庆, 孙耕耘, 沈玉先. 氯美昔布诱导肺癌细胞凋亡的作用机制[J]. 中国临床药理学与治疗学, 2012, 17(1): 47-51.

HAO Ji-qing, SUN Gen-yun, SHEN Yu-xian. Mechanisms of lumiracoxib on apoptosis in human lung cancer cells[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2012, 17(1): 47-51.

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