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1、Toll樣辦3獻(xiàn)鼠急用刪2018-03-2001:26:12中國現(xiàn)代醫(yī)生2018年1期王媛媛曹建鄧?yán)颍壅＃蒴Y的研宂Toll樣受體3(TLR3)在大鼠心肌梗死屮的表達(dá)及作用機(jī)制。方法制備TLR3基因敲除大鼠及野生型大鼠，采用球囊結(jié)扎冠脈方法制作心肌梗死動物模型。隨機(jī)分為野生型假手術(shù)組(n=15)、野生型心肌梗死組(n=15)、(TLR3-/-)假手術(shù)組(n=15)、(TLR3-/-)心肌梗死組(n=15)。檢測心肌組織肌酸激酶同工酶(CK-MB)、肌鈣蛋白cTnl含雖；通過Westernblot
2、法檢測Toll樣受體3、NF-kB表達(dá)。結(jié)果與野生型心肌梗死組大鼠比較，(TLR3-/-)心肌梗死組反映心肌損傷的CK-MB、cTnl減低；NF-kB表達(dá)降低；各組間差異均有統(tǒng)計學(xué)意義(P<0.05)。結(jié)論TLR3S因缺失在急性心肌梗死中A?有心臟保護(hù)作用，其保護(hù)機(jī)制與下調(diào)NF-kB衣達(dá)，減輕心肌梗死炎癥反應(yīng)有關(guān)。［關(guān)鍵詞］TOLL樣受體3;急性心肌梗死；核因子-kB;棊因敲除［中圖分類號］R541;R392［文獻(xiàn)標(biāo)識碼】A［文章編號］1673-9701(2018)01-0036-03Mecha
3、nismofToll-likereceptor3inacutemyocardialinfarctioninratsWANGYuanyuanlCAOJian2DENGLi11.DepartmentofCardiology，theThirdHospitalofNanchang，Nanchang330009，China；2.DepartmentofAnesthesiology,theSecondAffiliatedHospitalofNanchangUniversity,Nanchang，330006
4、，China［Abstract］ObjectiveTostudytheexpressionofToll-likereceptor3(TLR3)inmyocardialinfarctionofratsanditsmechanism.MethodsTLR3geneknockoutratsandwild-typeratswereprepared.Animalmodelsofmyocardialinfarctionwerecreatedbyballoonligationofcoronaryarterie
5、s.Theratswererandomlydividedintowild-typeshamsurgerygroup(n=15),wild-typemyocardialinfarctiongroup(n=15),(TLR3-/-)shamsurgerygroup(n=15),and(TLR3-/-)myocardialinfarctiongroup(n=15).Thecreatinekinase(CK-MB)andtroponincTnlcontentsinmyocardialtissueswer
6、emeasured.Toll-likereceptor3andNF-kBexpressionsweredetectedbyWesternblotmethod.ResultsComparedwiththeratsinthewild-typemyocardialinfarctiongroup，thelevelsofCK-MBandcTnlwhichreflectedmyocardialinjuryinthe(TLR3-/-)myocardialinfarctiongroupweredecreased
7、；NF-kBexpressionwasdecreased；thedifferencesbetweengroupswerestatisticallysignificant(P<0.05).ConclusionTLR3genedeletionhascardioprotectiveeffectsinacutemyocardialinfarction.Itsprotectivemechanismisrelatedtothedown-regulationofNF-kBexpressionandallevi
8、ationofinflammatoryresponseinducedbymyocardialinfarction.［Keywords］TOLL-likereceptor3；Acutemyocardialinfarction；NF-kB；Geneknockout急性心肌梗死是嚴(yán)重危害人類健康的常見疾病之一，研允表明，在心肌梗死沿，心肌組織會分泌大S炎性因子(如白細(xì)胞介素)，炎癥因子局部W?常表達(dá)及不適當(dāng)堆積可激活細(xì)胞毒性T細(xì)胞造成心肌細(xì)胞的結(jié)構(gòu)和功能障礙，與心室重塑密切相關(guān)［1-3］。此外還可引起
