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1、四川大学学报(医学版)2004;35(2):188190JSichuanUniv(MedSciEdi)大鼠抗Thy1系膜增生性肾小球肾炎3模型发病机制探讨112111张克非,张亮,吴雄飞,张祥贵,于泓,赵士启1.遵义医学院附属医院肾病风湿科(遵义563003);2.第三军医大学附属西南医院肾科【摘要】目的探讨大鼠抗Thy1系膜增生性肾炎模型发病机制。方法制备兔抗大鼠胸腺细胞免疫血清(ATS),再将ATS经尾静脉注射给模型组Wistar大鼠,诱导其发生系膜增生性肾炎(MsPGN);另设正常对照组,静脉注射生理盐水。隔天测定24h尿蛋白定量,放免法测定血清细胞
2、因子含量,显微镜观察肾脏系膜组织增殖程度,BI2000图像分析系统对肾小球系膜区进行分析。分别于注射ATS后1、3、5及7d各时间点处死模型组大鼠6只。结果模型组与对照组比较,尿量、饮水量变化无显著性差异(P>0.05);模型组1、3、5及7d尿蛋白定量与对照组相应时间点比较均明显升高(P<0.001～0.005);各时间点大鼠血清IL21、IL26及TNF含量均高于对照组(P<0.001～0.005);模型组肾小球系膜细胞及基质明显增生。结论细胞因子可能在鼠抗Thy1肾炎模型的发病中起重要作用。【关键词】抗Thy1系膜增生性肾炎发病机制【中图分类号】R6
3、92.3PathogenesisofRatMesangialProliferativeGlomerulonephritisInducedbyAnti-Thy1AntibodyZHANGKe2fei,ZHANGLiang,WUXiong2fei,ZHANGXiang2gui,YUHong,ZHAOShi2qi.DepartmentofNephrology,TheFirstAffiliatedHospitalofZunyiMedicalCollege,Zunyi563003,China【Abstract】ObjectiveToprobeintothepatho
4、genesisofratmesangialproliferativeglomerulonephritis(MsPGN)inducedbyanti2Thy1antibody.MethodsAnti2Thy1serumwasproduced,andthenintravenouslyinjectedintoWistarratsforestablishinganexperimentalmodelofMsPGN.Thecontrolgroupreceivedintravenousinjectionofnormalsaline.Urinaryvolumeandurin
5、aryproteinwereexaminedeveryotherday.TheIL21,IL26andTNFcontentsofserumweredetectedbyradioimmunoassay.PathologicmorphologyofrenalsectionwasobservedwithmicroscopeandBI2000ImageAnalysisSystem.Theratsofmodelgroupwerekilledonthe1st,3rd,5thand7thdays.ResultsNosignificantdifferencewasseen
6、betweenthemodelgroupandcontrolgroupinregardtothevolumeofurineandin2takewater(P>0.05).Thelevelsofurinaryprotein,IL21,IL26andTNFinmodelgroupweresignificantlyhigherthanthoseincontrolgroupatalltimepoints(P<0.00120.005).Glomerularmesangiumcellsandmatrixinthemodelgroupwereobviouslyproli
7、ferative,comparedwiththoseincontrolgroup.ConclusionItissuggestedthatcytokineplaysanimportantroleintheonsetofMsPGN.【Keywords】Anti2Thy1MesangilproliferativeglomerulonephritisPathogenesis大鼠胸腺细胞抗体诱发大鼠系膜增生性肾炎健康雄性新西兰大白兔,4周龄(4只)及6～8(mesangialproliferativeglomerulonephritis,周龄(30只)健康雄性Wis
8、tar大鼠,由第三军医大MsPGN)是目前被广泛应用并公认比较典型
