摘要
目的探讨氯美昔布(lumiracoxib,LUM)抗肺癌作用的可能机制。方法采用Western blot法检测不同浓度的LUM作用于A549和NCI-H460细胞COX-2表达及放射免疫法(RIA)检测PGE2及cAMP水平。结果A549细胞中随着LUM浓度的增加,COX-2的表达水平逐渐下降。而NCI-H460细胞中不同剂量组间COX-2的表达水平并无明显的变化。不同浓度的LUM作用于A549和NCI-H460细胞后,发现PGE2的水平下降、cAMP的水平升高均呈剂量依赖性(P<0.01)。结论LUM在体外的抗肺癌细胞增殖作用机制可能涉及到COX-2依赖性和非依赖性两种途径,并通过PGE2的合成减少和cAMP的水平升高来实现的。
Aim To investigate the possible mechanism of antitumor in human lung cancer cell lines A549 and NCI-H460 induced by lumiracoxib. Methods The expression of COX-2 was detected by Western blot and the levels of PGE2 and cAMP was determined by radio- immunoassay （RIA）. Results COX-2 protein was highly expressed in A549 and NCI-H460 ceils. After treatment with 15 -240 μmol ·L^-1 LUM for 24 hrs, LUM significantly decreased the level of COX-2 in A549 cells, but not in NCI-H460 cells. Compared with the control, the PGE2 production was reduced and the level of cAMP was increased after the treatment with 15,30, 60,120,240 μmol · L^-1 of LUM, respectively. Conclusion The effect of Lumiracoxib on antitumor is in COX-2-dependent or-independent manner. The antitu- mor effect of LUM may be related to inhibiting the COX-2 activities by decreasing its secretion, up-regulating the level of cAMP, and down-regulating the level of PGE2.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2009年第7期920-923,共4页
Chinese Pharmacological Bulletin
基金
安徽省教育厅自然科学研究项目省级一般资助项目(NoKJ2007B142)
安徽省科技厅科研计划资助项目(No07021008)
