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1、復(fù)方861對(duì)腎臟纖維化防治作用及其機(jī)理的實(shí)驗(yàn)研究摘要目的采用大鼠糖尿病腎病模型和腎小球硬化模型研究中藥復(fù)方861抗腎臟纖維化的作用和機(jī)理。方法實(shí)驗(yàn)大鼠摘除右腎以加速腎損傷的發(fā)生。分別采用鏈尿佐菌素(STZ)腹腔注射和阿霉素(ADR)尾靜脈重復(fù)注射制備糖尿病腎病模型和腎小球硬化模型。治療組以復(fù)方861灌胃治療。用腎組織病變半定量積分評(píng)價(jià)腎損傷程度;檢測(cè)血生化指標(biāo)和尿蛋白排泄量以從器官水平觀察療效;腎小球硬化模型動(dòng)物用腎組織Col-N,FN和LN免疫組化染色表明細(xì)胞外基質(zhì)(ECM)的沉積量。通過(guò)以下途徑探討復(fù)方861抗腎臟纖維化的
2、作用機(jī)理:(1)糖尿病腎模型設(shè)血管緊張素受體拮抗劑氯沙坦陽(yáng)性對(duì)照組;(2)腎小球硬化模型用免疫組化技術(shù)檢測(cè)轉(zhuǎn)化生長(zhǎng)因子(TGF)-131蛋白水平的表達(dá)。結(jié)果1.復(fù)方861可改善糖尿病腎病大鼠的肌配清除率、減少尿白蛋白含量、控制高血壓以及明顯減輕系膜基質(zhì)增生，與氯沙坦陽(yáng)性對(duì)照組比較無(wú)顯著差異。2腎小球硬化模型861治療組腎組織損害半定量積分明顯低于硬化組，ECM(Col-IV,FN和LN)蛋白沉積和TGF-D1蛋白水平的表達(dá)均顯著低于硬化組伊<0.001)9結(jié)論1摘除一側(cè)腎臟后，STZ誘導(dǎo)的糖尿病腎病模型和ADR誘導(dǎo)的腎小球硬化
3、模型均可發(fā)生腎小球硬化和腎小管一間質(zhì)纖維化。后者病變程度較重。2復(fù)方861對(duì)糖尿病大鼠具有延緩糖尿病腎病進(jìn)展的腎臟保護(hù)作用，并能明顯減輕腎小球硬化和腎小管一間質(zhì)纖維化的損傷程度，減少ECM的異常沉積。3.本試驗(yàn)結(jié)果提示，復(fù)方861抗腎臟纖維化的機(jī)理可能與下調(diào)TGF-01的表達(dá)，以及抑制AngI介導(dǎo)的TGF-H1產(chǎn)生增加引起的ECM合成增加有關(guān)。關(guān)鍵詞復(fù)方861腎小球硬化糖尿病’腎病細(xì)胞外基質(zhì)轉(zhuǎn)化生長(zhǎng)因子一01TherapeuticeffectofCpd.861onrenalfibrosisanditsmechanisminra
4、tsAbstractObjectiveToexplorethemechanismofameliorativeeffectofChinesetraditionalmedicinecompound861(Cpd.861)onrenalfibrosisinuninephrectomizedratsofStreptozotocin(STZ)-induceddiabeticnephropathyandAdriamycin(ADR)一inducedglomerulo-sclerosis.MethodEfectofCpd861wasobse
5、rvedinanimalmodelsofSTZ-induceddiabeticnephropathyandADR-inducedglomerulo-sclerosis.Losartanwasusedaspositivecontrolindiabeticrats.Biochemistryindex,urinaryproteinandrenalpathologicalchangeswereassessedinallexperimentalanimals.Theexpressionoftransforminggrowthfactor
6、(TGF)la1andextracellularmatrix(ECM)proteinCol-IV,FNandLNwereanalyzedbyimmuno-histochemistryinglomerulosclerosisrats.Results1.1ndiabeticrats,Cpd861couldcorrectelevatedurinaryalbuminandhypertension,improvecreatinineclearanceandreducetheproliferationofmesangialmatrix.T
7、herewasnosignificantdifferencebetweenCpd861treatedgroupandLosartantreatedgroup.2.1nglomerulosclerosisrats,Cpd861treatedgrouphadsignificantlylowerintegralofdegreeinrenaldamage(P<0.001).ThedepositionofECMproteinandtheexpressionofTGF-ID1proteininCpd861treatedgroupwerem
8、uchlowerthanscleroticgroup(P<0,001)Conclusion1.TheanimalmodelsofSTZ-induceddiabeticnephropathyandADR-inducedglomerulosclerosisbothcanprese
