慢性肾衰大鼠肾脏细胞凋亡、凋亡相关基因表达及苯那普利干预作用研究.pdfVIP

4.TUNEL显示5/6肾切除大鼠肾脏凋亡细胞数增加，但苯那 普利治疗组较非治疗组凋亡细胞数少。 5。免疫组织化学染色显示 5/6’肾切除大鼠肾脏抗 Bax蛋白 及抗 IV型胶原抗体反应表达增强;苯那普利治疗组较非治疗 组，Bax蛋白表达下调，抗IV型胶原抗体染色反应减弱。 6.流式细胞术定量检测结果表明，5/6肾切除大鼠肾脏细胞 凋亡率升高，Bcl-2,Bax,Fas-L及Fas表达增强。苯那普利治 疗能够降低肾脏细胞的 ，下调Bax,Fas及Fas-L表达， 同时可上调Bcl-2表达 结论:1.细胞凋亡可能参与子漫性肾功能衰竭肾小球硬化和 肾小管萎缩、间质纤维化的病理过程。 2.血管紧张素转换酶抑制剂苯那普利的肾功能保护作用可能 部分是通过影响肾脏细胞凋亡及凋亡相关基因实现的。 关键词:慢性肾功能衰竭 细胞凋亡 凋亡相关基因蛋白 血管紧张素转换酶抑制剂 Apoptosisandtheeffectsofbenazeprilonapoptosisin thekidneysofratswithchronicrenalfailure Abstract Objectives:Toinvestigateapoptosisandtheexpressionof apoptoticregulatoryproteinsFas-L,Fas,BaxandBcl-2aswellasthe effectsofangiotensinconvertingenzymeinhibitorbenazeprilon apoptosisandtheexpressionofapoptoticregulatoryproteinsinthe kidneysofratswithchronicrenalfailure. Methods:Chronicrenalfailurewasinducedinthirty-twoadult maleSDratsby5/6nephrectomy.Theanimalsweredividedinto threegroups:A).5/6nephrectomygroup;B).benazepril-treated groupwith5/6nephrectomy;C).Shamoperatedgroup.Theanimals werekilledatweek6andweek12aftersurgery.Residualkidneys wereexaminedbymeansoflightmicroscopy,electronmicroscopy, immunohistochemicalstaining,TUNEL andflow cytometry, combiningwithexaminationofrenalfunction,inordertoobservethe changesofrenalfunctionandrenalmorphology,aswellasapoptosis andtheexpressionofapoptoticregulatoryproteins. Results:1.Thelevelsof24-hoururinaryproteinexcretion, serumcreatinineandBUNincreasedin5/6nephrectomyratsatweek 6.Itismoreprominentatweek12.Therenalfunctionwasimproved inbenazepril-treatedgroup,comparingwithnon-treatedgroup. 2.Lightmicroscopically,mostglomerulishowedcompensatory hypertrophywithexpansionofmesangialmatrixandincreaseofcell numberatweek6aftersurgery.Tubuleatrophywasoccasionally observed.Atweek12,theremnantkidneyshowedextensive 3 glomeurlarscleroticlesionconsistingofdeposi