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AbstractObjectiveToinvestigatetheeffectsof3-hydroxy一3-methylglutaryl(删G)-CoAreductaseinhibitorfluvastatinandangiotensinIIantagonistlosartanonlectinlikeoxidizedlowdensitylipoproteinreceptor一1expressioninkidneysandaortasofratremnantkidneymodel.ToexploretheeffectsofLOX一1inchronickidneydisease(CKD)andthemechanismthatunderliesstatinsandangiotensinItantagonistsretardingtheprogressionofCKD.MethodsAmong358-week—oldSprague—Dawleyrats,28wererandomlyselectedtoperformremnantkidneymodeloperationand7wereshamoperatedasnormalcontr01.Remnantkidneyratswererandomizedinto4groups:remnantkidneymodelgroup,fluvastatintreatedgroup,losartantreatedgroupandcombined-treatmentgroup.Oneweekaftertheoperation,fluvastatin(15mg/kgd)wasadministereddailybygavagetotheratsinfluvastatintreatedgroup,losartan(30mg/kg?d)inlosartantreatedgroup,andfluvastatin(15mg/kg?d)combinedwithlosartan(30mg/kg?d)incombined—treatmentgroup.Waterwasgiventotheratsinremnantkidneymodelgroupandcombined-treatmentgroupbygavage.8weekslater,urinewascollectedand24hurineproteinwastestedbeforetheratswerekilled.Bloodwasdrawnfromaortasandthenserumureanitrogen,creatinine,cholesterolandtriglyerideweremeasured.LOX-1andMCP一1expressioninkidneyswereevaluatedbyRT—PCR,LOX-Iexpressioninkidneysandaortasweredeterminedbyimmunohistochemistryandhistologicalchangesinkidneysweredetectedbypathologicalexamination.ResultsComparedwithshamgroup,serumcreatinine,cholesterol,triglyerideandurineproteinweremarkedlyincreasedinremnantkidneymodelgroup(尺0.01).Comparedwithremnantkidneymodelgroup,serumcreatinine,cholesterol,triglyerideandurineproteinweresignificantlyamelioratedinfluvastatintreatedgroup,losartantreatedgroupandcombined—treatmentgroup(尺O.05),butshowednosignificantdifferencebetweenfluvastatintreatedgroupandlosartantreatedgroup(乃0.05).TheresultofRT—PCRshowedthatLOX一1andMCP-ImRNAexpressionweredramaticallyup-regulatedinremnantkidneymodelgroup(P(O.05),andfluvastatinandlosartangreatlydown—regulatedtheexpressionofLOX-IandMcP_1(尺0.05),coadministrationoffluvastatin
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