基于肺肠微生态和mekerk信号通路探讨肺与大肠病理传变的生物学基础-study on biological basis of pathological changes of lung and large intestine based on microecology of lung and intestine and mekerk signal pathway.docx
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基于肺肠微生态和mekerk信号通路探讨肺与大肠病理传变的生物学基础-study on biological basis of pathological changes of lung and large intestine based on microecology of lung and intestine and mekerk signal pathway
.肠病大鼠的肺组织和结肠组织的MEK/p-MEK和ERK/p-ERK蛋白变化具有较为一致的趋势,一定程度上体现了肺肠之间的同步变化。提示MEK/ERK通路可能是“肠病及肺”的生物学基础之一。.肺病大鼠可出现肺肠TNF-α受体、IL-1β受体和c-Fos含量的同步动态变化,或在肺肠同步减少,或在肺减少而在肠增多。提示TNF-α受体、IL-1β受体和c-Fos可能是“肺病及肠”的部分物质基础。.肠病大鼠可出现肺肠TNF-α受体、IL-1β受体和c-Fos含量的同步动态变化,或在肺肠同步减少,或在肠减少而在肺增多,或在肠增多而在肺减少。提示TNF-α受体、IL-1β受体和c-Fos可能是“肠病及肺”的部分物质基础。关键词:肺病及肠;肠病及肺;肺肠传变;肺与大肠相表里;菌群;MEK/ERK信号通路;TNF-α受体;IL-1β受体;c-FosABSTRACTObjective:Toestablishpulmonarydisease(chronicbronchitis)andboweldisease(ulcerativecolitis)animalmodelsrespectively,whicharebothchronicnon-specificinflammatorydisease.Selectthreedifferentpoints,synchronousobservetherespiratoryandintestinalmicroflora,MEK/ERKsignalpathway,anditsupstreammediatorsofinflammationreceptorTNF-alphareceptor,IL-1betareceptorsanddownstreameffectersubstancesC-FOSbothinlungandlargeintestine,toexplorethebiologicalbasisofthemasschangeofthelungandlargeintestineinpathologicalstate.Method:Usesmokedmethodtocopypulmonarydisease(chronicbronchitis)ratmodel,takesamplesoflungandintestinalsynchronousdynamicobservationrespectivelyatmodel20th,50thand70th.UseTNBScombinedethanolmethodtocopyboweldisease(ulcerativecolitis)ratmodel,takesamplesoflungandintestinalsynchronousdynamicobservationrespectivelyatmodel8th,29thand50th.Detectthetotalnumberofaerobicbacteria,totalnumberofanaerobicbacteria,E.coli,enterococci,staphylococcusaureus,clostridiumperfringens,bifidobacteriumandlactobacillusbothinrespiratoryandintestinalatthesametime.DetectMEK,p-MEK,ERK1/2,p-ERK1/2proteinexpressioninthehomogenateoflungtissueandcolontissuebyWestern-Blotmethod.UseELISAmethodtodetectthecontentofTNF-alphareceptor,IL-1betareceptorandC-FOSinthehomogenatesoflungtissueandcolontissue.Results:Respiratoryandintestinalflora:Pulmonarydisease(CB)modelratshavedifferentdegreechangesoffloraspeciesandquantitiesateachtimepointintherespiratoryandintestinal.Atmodel20th,thetotalnumberofaerobicbacteriaintherespiratoryandintestinalincreasedsimultaneously.Intestinalmicrobialcolonizationresistance(B/E)decreasedsignificantly.Thetotalnumberofae
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