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时间:2018-12-03
《toll样受体3在大鼠急性心肌梗死中的作用机制》由会员上传分享,免费在线阅读,更多相关内容在学术论文-天天文库。
1、Toll样辦3献鼠急用刪2018-03-2001:26:12中国现代医生2018年1期王媛媛曹建邓莉[摘耍]鬥的研宂Toll样受体3(TLR3)在大鼠心肌梗死屮的表达及作用机制。方法制备TLR3基因敲除大鼠及野生型大鼠,采用球囊结扎冠脉方法制作心肌梗死动物模型。随机分为野生型假手术组(n=15)、野生型心肌梗死组(n=15)、(TLR3-/-)假手术组(n=15)、(TLR3-/-)心肌梗死组(n=15)。检测心肌组织肌酸激酶同工酶(CK-MB)、肌钙蛋白cTnl含虽;通过Westernblot
2、法检测Toll样受体3、NF-kB表达。结果与野生型心肌梗死组大鼠比较,(TLR3-/-)心肌梗死組反映心肌损伤的CK-MB、cTnl减低;NF-kB表达降低;各组间差异均有统计学意义(P<0.05)。结论TLR3S因缺失在急性心肌梗死中A•有心脏保护作用,其保护机制与下调NF-kB衣达,减轻心肌梗死炎症反应有关。[关键词]TOLL样受体3;急性心肌梗死;核因子-kB;棊因敲除[中图分类号]R541;R392[文献标识码】A[文章编号]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急性心肌梗死是严重危害人类健康的常见疾病之一,研允表明,在心肌梗死沿,心肌组织会分泌大S炎性因子(如白细胞介素),炎症因子局部W•常表达及不适当堆积可激活细胞毒性T细胞造成心肌细胞的结构和功能障碍,与心室重塑密切相关[1-3]。此外还可引起
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