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1、摘要結(jié)論：1.本研究建立以BSA+CCl4+LPS誘導(dǎo)的大鼠IgAN模型，并發(fā)現(xiàn)TIM-1mRNA的表達(dá)上調(diào)，且與IgAN大鼠的24尿蛋白定量，腎臟病理組織學(xué)損傷程度正相關(guān)，提示TIM-1信號通路可能參與大鼠IgAN的發(fā)病及進(jìn)展。2.IgAN大鼠腎組織中TIM-1與IL-4表達(dá)均上調(diào)并呈正相關(guān)，提示TIM-1信號通路可能參與調(diào)控Th2優(yōu)勢反應(yīng)，而參與IgAN的發(fā)病。3.IgAN大鼠腎組織中TIM-1的表達(dá)與IFN-γ/IL-4表達(dá)呈負(fù)相關(guān)，提示TIM-1信號通路可能通過調(diào)控Th1/Th2平衡來參與IgAN的發(fā)病。關(guān)鍵詞：IgA腎病；TIM-1；IL-4；IFN-
2、γ；FOXP3IVAbstractABSTRACTObjective:TostudytherelationshipbetweenT-cellimmunoglobulindomainandmucindomain-1(TIM-1)andTcellsubsetsinIgAnephropathy(IgAN)ratsandnormalrats,andtoexploremechanismofTIM-1signalingpathwayactinIgANpathogenesis.Method:1.EstablishexperimentalmodelofIgANrat:20SDm
3、aleratswererandomlydividedintoIgANmodelgroupandnormalcontrolgroup.IgANmodelgroupweresubcutaneouslygivento0.1%bovineserumalbumin(BSA)intragastriceveryotherday+CCL4mixturedwithcastoroilperweek+lipopolysaccharide(LPS)tailveininjectiontwicetoestablisharatmodelofexperimentalIgAN;andnormal
4、controlgroupweretreatedwithequalvolumeofPBSandsaline.2.IdentificateIgANratsmodelandobserveindexesduringexperiment:Toobservegeneralconditionsandotherindicatorsofratsincluding24hurinaryprotein,serumalbumin,serumcreatinine.ratswerekilledinthe9thweekendandratskidneywerekeptforHEandimmuno
5、fluorescence.partsofthekidneytissuesweregainedforreal-timequantitative,andimmunohistochemicalmethodsforTIM-1、IL-4、IFN-γandFOXP3expression.3.Comparekidneypathologicallesion,immunohistochemicalexpressionandTIM-1mRNAexpressionbetweenthetwogroups.AnalysisTIM-1expressionandclinicalorpatho
6、logicaldatainIgANgroup.Result:1.Thegeneralconditionsbetweentwogroups;IgANmodelgrouphadnosignificantdifferencefromcomparisoncontrolgroupatthebeginning.Lackingofexercise,weightgainslowingdownwerehappendedinthe6thweekend,andgotworseinthe8thweekend.Comparedwithcontrastcontrolgroupweightg
7、ain,weightgaininIgANratshadbeensignificantlysloweddownsincethe6thweekend,thedifferencewasnotstatisticallysignificant(P<0.01).2.ThekidneypathologyandrenaldamageRatingofrats:VAbstractIgAimmunofluorescenceofnormalcontrolgroupwasnegative,withlightchangeinglomerularandtubularstructure.Dif
8、ferentdegree
