中文摘要：

目的：研究喹诺酮类抗生素莫西沙星（moxifloxacin，MXF）对铜绿假单胞茵（Reudomonasaeruginosa，PA）诱导气道上皮细胞表达产黏蛋白MUC5AC的影响，并探讨其可能的分子机制。方法：体外培养NCI．H292细胞，用不同浓度的PA、产藻酸盐型PA脂多糖（光滑型，SPA-LPS）、非藻酸盐型PA脂多糖（粗糙型。rPA-LPS）刺激。然后加入不同浓度MXF孵育24h，分别采用ELISA和实时定量PCR检测MUC5AC蛋白和mRNA的表达情况，Westernblot检测NCI．H292细胞内ERK1／2的激活情况。结果：PA、SPA-LPS和rPALPS能明显诱导NCI-H292细胞产生和表达MUC5AC．并能促进ERK1／2磷酸化。而MXF处理后，能以剂量依赖性方式抑制PA、SPA-LPS或rPA-LPS诱导的MUC5AC蛋白表达，并有效抑制ERK1／2的磷酸化。结论：MXF能抑制PA诱导的黏蛋白表达。因此有望用于PA诱导的黏蛋白过度分泌的治疗。

英文摘要：

Objective To investigate the effect of fluoroquinolone＇s antibiotics moxifloxacin （MXF） on Pseudomonas aeruginosa （PA）-induced mucus MUCSAC expression in airway epithelial cells. Methods NCI-H292 cells were stimulated with PA, lipopolysaccharide from alginate producing PA （smooth, sPA-LPS） and non-alginate producing PA （rough,rPA-LPS） respectively for 24 h in vitro. MXF was added in different concentrations. Expressions of MUC5AC gene and mucin protein was quantified by ELISA and real time PCR respectively, while phosphorylation of ERK1/2 was detected by Western blot. Results PA, sPA-LPS or rPA-LPS could significantly induce MUC5AC gene and protein expression in NCI-H292 cells,also phosphorylate ERK1/2,and MXF could significantly inhibit it. Conclusion MXF can attenuate PA-induced mucus expression in human airways and may be used for treating PA-induced mucus hypersecretion in clinical practice.