孟鲁司特抑制哮喘模型大鼠气道黏液高分泌  

Montelukast inhibits hypersecretion of airway mucus in asthmatic rats

作　　者：张博达[1] 李俊玲 金典 陈思敏 董艳[2] ZHANG Bo-da;LI Jun-ling;JIN Dian;CHEN Si-min;DONG Yan(the Affiliated Hospital of North Sichuan Medical College,Nanchong 637000;Hospital of Chengdu University of Traditional Chinese Medicine,Chengdu 610075,China)

机构地区：[1]川北医学院附属医院,四川南充637000 [2]成都中医药大学附属医院,四川成都610075

出　　处：《基础医学与临床》2019年第12期1699-1703,共5页Basic and Clinical Medicine

基　　金：四川省科技厅科技攻关计划(2014SZ-0071)

摘　　要：目的探讨白三烯(LTs)介导的炎性损伤对哮喘大鼠气道黏液高分泌的作用。方法用卵蛋白(OVA)经典造模方法复制哮喘大鼠模型,用白三烯特异性受体拮抗剂孟鲁司特行干预性治疗,并使用ELISA、Western blot和RT-qPCR等方法观察炎性反应及气道黏液分泌指标变化。结果孟鲁司特可抑制CysLTs受体1(P<0.05),抑制P38MAPK磷酸化(P<0.05),下调MUC5AC基因表达及蛋白合成(P<0.05)。结论白三烯介导的炎性反应在哮喘大鼠模型中有促进气道黏液高分泌的作用,这一作用能被孟鲁司特所抑制。Objective To investigate the effect of leukotriene-mediated inflammatory injury on hypersecretion of airway mucus in asthmatic rats.Methods The rat model of asthma was duplicated with OVA classic modeling method,and the CysLTs1 specific receptor antagonist montelukast was used for ELISA,Western blot and qPCR to observe the change of inflammation and airway mucus secretion indexes.Results Montelukast could inhibit CysLTs receptor 1,P38MAPK phosphorylation,and down-regulate MUC5AC gene expression and protein synthesis.Conclusions Leukotriene-mediated inflammation promotes airway mucus hypersecretion in asthmatic rats,which is antagonized by montelukase.

关 键 词：白三烯 孟鲁司特 哮喘 气道黏液高分泌 

分 类 号：R915[医药卫生—微生物与生化药学]