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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。
Objective To investigate the effects of esomeprazole on LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in RAW 264.7 mouse macrophages. METHODS RAW 264.7 mouse macrophages were cultured in vitro and treated with 15 μg / ml esomeprazole for 2 h before LPS stimulation. The production of NO and PGE2 was detected by ELISA. The generation of reactive oxygen species (ROS) was detected by fluorescence spectrophotometer. The expression of P-ATP was detected by RT-PCR and the activity of NADPH oxidase was determined by colorimetric assay. Results Esomeprazole significantly inhibited NO and PGE2 production in mouse macrophages induced by LPS, but had no effect on the expression of P-ATPase. In addition, esomeprazole also significantly inhibits ROS production and inhibits NADPH oxidase activity. NADPH oxidase inhibitor DPI can reduce NO and PGE2 levels, ROS inhibitor NAC treatment can inhibit the production of NO. Conclusion Esomeprazole inhibits LPS-induced NO secretion in RAW 264.7 cells by inhibiting NADPH oxidase activity and ROS production. Although esomeprazole also inhibits PGE2 production, it has little to do with ROS.