tim1信号通路在iga肾病大鼠发病机制中的作用

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1、-------摘要结论：1.本分析建立以BSA+CCl4+LPS诱导的大鼠IgAN模型，并发现TIM-1mRNA的表达上调，且与IgAN大鼠的24尿蛋白定量，肾脏病理组织学损伤程度正相关，提示TIM-1信号通路可能参与大鼠IgAN的发病及进展。2.IgAN大鼠肾组织中TIM-1与IL-4表达均上调并呈正相关，提示TIM-1信号通路可能参与调控Th2优势反应，而参与IgAN的发病。3.IgAN大鼠肾组织中TIM-1的表达与IFN-γ/IL-4表达呈负相关，提示TIM-1信号通路可能通过调控Th1/Th2平

2、衡来参与IgAN的发病。关键词：IgA肾病；TIM-1；IL-4；IFN-γ；FOXP3IV-----------AbstractABSTRACTObjective:TostudytherelationshipbetweenT-cellimmunoglobulindomainandmucindomain-1(TIM-1)andTcellsubsetsinIgAnephropathy(IgAN)ratsandnormalrats,andtoexploremechanismofTIM-1signalingp

3、athwayactinIgANpathogenesis.Method:1.EstablishexperimentalmodelofIgANrat:20SDmaleratswererandomly dividedintoIgANmodelgroupandnormalcontrolgroup.IgANmodelgroupwere subcutaneouslygivento0.1%bovineserumalbumin(BSA)intragastriceveryother day+CCL4mixturedwit

4、hcastoroilperweek+lipopolysaccharide(LPS)tailvein injectiontwicetoestablisharatmodelofexperimentalIgAN;andnormalcontrol groupweretreatedwithequalvolumeofPBSandsaline.2.IdentificateIgANratsmodelandobserveindexesduringexperiment:To observegeneralconditions

5、andotherindicatorsofratsincluding24hurinaryprotein, serumalbumin,serumcreatinine.ratswerekilledinthe9thweekendandratskidney werekeptforHEandimmunofluorescence.partsofthekidneytissuesweregained forreal-timequantitative,andimmunohistochemicalmethodsforTIM-

6、1、IL-4、IFN-γ andFOXP3expression.3.Comparekidneypathologicallesion,immunohistochemicalexpressionand TIM-1mRNAexpressionbetweenthetwogroups.AnalysisTIM-1expressionand clinicalorpathologicaldatainIgANgroup.Result:1.Thegeneralconditionsbetweentwogroups;IgANm

7、odelgrouphadnosignificantdifferencefromcomparisoncontrolgroup atthebeginning.Lackingofexercise,weightgainslowingdownwerehappendedin the6thweekend,andgotworseinthe8thweekend.Comparedwithcontrastcontrol groupweightgain,weightgaininIgANratshadbeensignifican

8、tlysloweddownsince the6thweekend,thedifferencewasnotstatisticallysignificant(P<0.01). 2.ThekidneypathologyandrenaldamageRatingofrats:V-----------AbstractIgAimmunofluorescenceofnormalcontrolgroupwasnegative,withlightchangei