埃索美拉唑抑制LPS诱导小鼠巨噬细胞产生NO和PGE_2  

Esomeprazole inhibits LPS-induced nitric oxide and prostaglandin E_2 production in murine macrophage RAW 264.7 cells

作　　者：何涛[1] 陈宏辉[1] 王正根[1] 

机构地区：[1]南华大学附属第二医院消化内科,衡阳421001

出　　处：《免疫学杂志》2014年第1期61-64,共4页Immunological Journal

摘　　要：目的研究埃索美拉唑对LPS诱导RAW 264.7小鼠巨噬细胞一氧化氮(nitric oxide,NO)和前列腺素E2(prostaglandin E2,PGE2)的影响。方法体外培养小鼠巨噬细胞RAW 264.7,LPS刺激前先用15μg/ml埃索美拉唑处理2 h,ELISA检测NO和PGE2的产生。荧光分光光度计检测活性氧(reactive oxygen species,ROS)产生;RT-PCR检测P-ATP的表达情况;比色法测定NADPH氧化酶活性。结果埃索美拉唑能显著抑制LPS诱导小鼠巨噬细胞产生NO和PGE2,但对P-ATP酶的表达无明显影响。此外,埃索美拉唑也能显著抑制ROS的产生,并抑制NADPH氧化酶活性。NADPH氧化酶抑制剂DPI可减少NO和PGE2水平,ROS抑制剂NAC处理能抑制NO的产生。结论埃索美拉唑通过抑制NADPH氧化酶活性以及ROS产生从而抑制LPS诱导RAW 264.7细胞分泌NO。虽然埃索美拉唑也能抑制PGE2产生,但与ROS关系不大。To investigate the inhibitory effects of Esomeprazole on LPS-induced production of nitric oxide （NO） and prostaglandin E2 （PGE2） in RAW264.7 cells, routine maerophage RAW 264.7 cells were cultured in vitro and incubated with 15 μg,/ml Esomeprazole. Then, the ceils were stimulated by LPS, and the production of NO and PGE2 were detected by ELISA. Furthermore, reactive oxygen species （ROS） was detected by fluorospectrophotometer methods; P-ATPase expression and NADPH oxidase activity were determined by RT-PCR and eolorimetry, respectively. ELISA results showed Esomeprazole could significantly inhibit LPS-induced NO and PGE2 production, but not exerted any effect on p-ATPase expression. In addition, Esomeprazole could also inhibit ROS production and NADPH oxidase activity. And DPI, an inhibitor of NADPH oxidase, could reduce the NO and PGE2 production, but NAC, a ROS scavenger, only inhibit NO secretion. All of these results demonstrated that Esomeprazole could inhibit LPS-indueed NO production via inhibiting ROS production and NADPH oxidase activity in RAW264.7 ceils, although Esomeprazole also inhibit PGE2 production, but it do not related with ROS.

关 键 词：埃索美拉唑 巨噬细胞 一氧化氮 前列腺素E2 NADPH氧化酶 

分 类 号：R965[医药卫生—药理学]