本文關(guān)鍵詞：TLR4與TLR9介導(dǎo)的信號(hào)傳導(dǎo)通路在炎癥性腸病中的作用研究，由筆耕文化傳播整理發(fā)布。

網(wǎng)友Horange近日為您收集整理了關(guān)于TLR4與TLR9介導(dǎo)的信號(hào)傳導(dǎo)通路在炎癥性腸病中的作用研究的文檔，希望對(duì)您的工作和學(xué)習(xí)有所幫助。以下是文檔介紹：3.6參考文獻(xiàn)304第二部分TLR4、TLR9在潰瘍性結(jié)腸炎結(jié)腸黏膜中的表達(dá)及意義——334.1前言4.2材料與方法4.3結(jié)果4.4討論盟結(jié)論4.6參考文獻(xiàn)4.7英漢縮略詞對(duì)照表4.8致謝5TOLL樣受體在炎癥性腸病發(fā)病機(jī)制中的作用(綜述)335822567333344444TLR4、TLR9在小鼠結(jié)腸炎腸黏膜中的表達(dá)及意義摘要1目的炎癥性腸病(Inflammatoryboweldisease,IBD)包括潰瘍性結(jié)腸炎(Ulcerativecolitis,UC)和克羅恩病(Crohndisease,CD)。近年來該病的發(fā)病率有逐漸增高的趨勢(shì),其病因和發(fā)病機(jī)制涉及遺傳、環(huán)境、免疫、感染等因素,但至今尚未闡明。新近研究發(fā)現(xiàn)Toll樣受體(Toll.1ikereceptors,TLRs)是參與非特異性免疫的一類重要分子,也是連接非特異性免疫和特異性免疫的重要橋梁。Toll樣受體屬于高度保守的I型跨膜蛋白(typeItransmembranceprotein),能識(shí)別病原相關(guān)分子模式(pathogenassociatedmolecularpatterns,PAMPs),通過髓樣分化因子88(m(來源：[])yeloiddifferentiationfactor88,MyD88).核因子rd3(nuclearfactor.rd3,NF.1cB)等多條信號(hào)途徑,啟動(dòng)細(xì)胞活化進(jìn)程,上調(diào)主要組織相容性復(fù)合物(plex,MHC)和共刺激分子表達(dá),分泌細(xì)胞因子等,從而進(jìn)一步誘導(dǎo)炎癥免疫反應(yīng),同時(shí)活化的TLRs也能激活T細(xì)胞,啟動(dòng)獲得性免疫反應(yīng)。本課題利用葡聚糖硫酸鈉(dextransulfatesodium,DSS)結(jié)腸炎模型研究結(jié)腸炎小鼠腸黏膜組織中TLR4、TLR9與NF.1cB及促炎癥細(xì)胞因子TNF.0【的表達(dá)以及相互關(guān)系,探討TLR4、TLR9信號(hào)途徑在實(shí)驗(yàn)性結(jié)腸炎中的作用。方法建立小鼠葡聚糖硫酸鈉結(jié)腸炎模型,進(jìn)行大體和組織病理學(xué)評(píng)價(jià):6.8周齡健康雄性Balb/c小鼠分為兩組:A組(正常對(duì)照組,n=5):蒸餾水自由飲用7天。B組(DSS急性結(jié)腸炎組,n=15):5%DSS溶液自由飲用7天。造模7天后處死小鼠,免疫組化方法檢測(cè)小鼠結(jié)腸黏膜TLR4、TLR9、3.TLR4和TLR9蛋白在DSS結(jié)腸炎小(來源：[])鼠結(jié)腸黏膜中的表達(dá)存在關(guān)聯(lián)并有較好的一致性,提示二者可能在DSS誘導(dǎo)小鼠結(jié)腸炎的發(fā)生、發(fā)展過程中起協(xié)同作用,共同促成及加劇了炎癥反應(yīng)的發(fā)生及持續(xù)。關(guān)鍵詞:炎癥性腸病;TLR4;TLR9;NF.r.B;免疫組織化學(xué):}I◆Abstract1ExpressionandsignificanceofTLR4,TLR9incolonicmucosainmicecolitisObjectiveInflammatoryboweldiseases(IBD)includeulcerativecolitis(UC)andCrohndisease(CD),whichhaveprogressivelyincreasedinthelast20years.ic,environmental,immunologic,infectiouscausesandetc,essinfndingtheaetiologicalculprit.IthasbeenfoundinrecentstudythatTLRisanimportantmo(來源：[])leculartoparticipateinnonspecificimmuneresponseandabridgefromnonspecifictospecificimmune.Toll-likereceptorsbelongstoafamilyoftypeItransmembranereceptors,theyboundtopathogenassociatedmolecularpatterns(PAMPS),throughmyeloiddifferentiationfactor88andnuclearfactor,induceactivation,upregulatemanymajorsignalpathways,theninitiatehlstoc。mpatlbllltyc。mplex‘yHc’cellandcostimulatorymoleculesexpression,secretecytokineandSOon.Atlast,theyinduceinflammationrespons(來源：[])e.ThepurposesofthisexperimentaretostudytheexpressionofTLR4,TLR9,NF—r.Bandn師一QincolonicmucosaofDSSinducedcolitisinanimalmodelanditsrelationshipwithpro-inflammatorycytokinesanditsmolecularregulatorymechanism,toexploretheeffectsofTLR4andTLR9signalpathwayontheexperimentalcolitis..-MethodsSettingupanimalmodelofDSScolitisandevaluatinggrosschangesand41.ThereweresignificantlyhigherexpressionofTLR4andTLR9inthecolonicmucosaofDSS-inducedmurinecolitis,whichtoso(來源：[])meextendreflectthedegreeofinflammation.2.TheexpressionofNF-r,BandTNF-paringtocontrolgroupwithaparalleledrelationtoTLR4andTLR9.ThedatawasreflectedtheP■expressionof:TLR4,TLR9,NF-rd3andpre—inflammatorycytokinesaref5弛^correlatedclosely.Theadditioneffectsofthemmayplayanimporta.ntroleinmagnifyingandsustainedinflammation.3.patibilityamongTLR4andTLR9,urrenceanddevelopmentprocessofInflammator

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  本文關(guān)鍵詞：TLR4與TLR9介導(dǎo)的信號(hào)傳導(dǎo)通路在炎癥性腸病中的作用研究，由筆耕文化傳播整理發(fā)布。