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时间:2020-03-03
《巨噬细胞炎性蛋白 1α在病毒性心肌炎小鼠中的表达及意义.doc》由会员上传分享,免费在线阅读,更多相关内容在工程资料-天天文库。
1、6.对照组MTP-la蛋白呈弱表达,心肌炎组小鼠于感染后7dMTP-la表达最明显,15〜30d其表达逐渐下降,但仍高于对照组(PV0.01或0.05),而3d与对照组比较,差异无显著性(P>0.05)7.心肌MIP-la蛋白表达水平与心肌病理积分的相关性:心肌炎组心肌MIP-la蛋白表达水平与心肌病理积分呈显箸正相关(尸0.82,P<0.05);8.血清MIP-la浓度与心肌病理积分的相关性:心肌炎组小鼠血清MIP-1a浓度与心肌病理积分呈显著正相关(尸0.89,户<0.05)。9.心肌炎组7〜30d各时点心肌IL・1[3、TNF-a含量较对照组显著升高(P<0.01),但3d与对照组比较,
2、差异无显著性(?>0.05)。结论1.MIP-la可能参与VM发病过程,其机制可能与促进炎症细胞向心肌浸润及增加IL-ip>TNF-a分泌有关;2.血清MTP-la浓度能反映心肌炎的严重程度,可作为心肌炎病情判断的一个血清学指标。关键词:巨噬细胞炎性蛋白Ta;病毒性心肌炎;白细胞介素-1卩;肿瘤坏死因子-aExpressionandSignificanceofMacrophageInflammatoryProtein-lainMurineViralMyocarditisAbstractObjectiveMacrophageinflammatoryprotein-1a(MIP-1a)9amemb
3、erofCCsubfamilyofchemokines,canspecificallyinducechemotaxisofinflammatorycellsincludingmonocytes,lymphocytesandneutrophils,therebybeinginvolvedinpathogenesisofavarietyofinflammatorydiseases.TheaimofthepresentstudywastoinvestigatethekineticfeaturesofMIP-laexpressioninmicewithviralmyocarditis(VM),andi
4、tsrolesinthepathogenesisofVM.Method:SeventyfiveBalb/cmicewererandomlydividedintotwogroups:themyocarditicgroupandacontrolgroup.Miceinthemyocarditicgroup(n=65)wereinoculatedintraperitoneallywith0」mLof1X102TCID50coxsackievirusB3(CVB3)dilutedinEagletminimalessentialmedium(EMEM)solution.Controlmiceweretr
5、eatedwith0」mLofEMEM・Afterweighingbodyweight(BW),10infectedmiceweresacrificedondays3,7,15and30postinoculation,andthecontrolmicewerekilledonday30postinoculation.Theheartswereremovedandweighedtocalculateheartweight(HW)/BW.Bloodwascentrifugatedtoobtainserum.Changesofmyocardialhistopathologywereexaminedt
6、hroughHEstain.ExpressionofMIP-lamRNAandproteininthemyocardiumwereexaminedbyRT-PCRandwesternblotting,respectively.SerumMIP-laconcentrations,myocardialinterleukin-1卩andtumornecrosisfactor-a(TNF・a)contentsweredetectedusingenzymelinkedimmunosorbentassay(ELISA).CorrelationanalysesbetweentheexpressionofMI
7、FproteinorscrumMIP-laconcentrationandmyocardialhistopathologicscoreswereinvestigated.Results1・Themortalityinmyocarditicgroupwas38.46%(25/65).Miceincontrolgrouphadnodeath.2.Myocardialmorphologywasnorma
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