ho1 nadph氧化酶在动脉粥样硬化性肾动脉狭窄肾组织中表达及药物干预-expression of ho1 nadph oxidase in renal tissue of atherosclerotic renal artery stenosis and drug intervention.docx

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ho1 nadph氧化酶在动脉粥样硬化性肾动脉狭窄肾组织中表达及药物干预-expression of ho1 nadph oxidase in renal tissue of atherosclerotic renal artery stenosis and drug intervention.docx

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ho1 nadph氧化酶在动脉粥样硬化性肾动脉狭窄肾组织中表达及药物干预-expression of ho1 nadph oxidase in renal tissue of atherosclerotic renal artery stenosis and drug intervention

结论：直接肾素抑制剂阿利吉仑与钙通道阻滞剂苯磺酸氨氯地平均能通过抑制动脉粥样硬化性肾动脉狭窄肾组织中氧化酶的产生并促进抗氧化接HO-1的表达来减少肾损伤，且通过实验结果得出阿利吉仑肾保护作用优于苯磺酸氨氯地平。关键词：直接肾素抑制剂；钙通道阻滞剂；血红素加氧酶-1；NADPH氧化酶；ARAS。TheexpressofHO-1andNADPHoxidaseinatheroscleroticrenalarterystenosisanddrugsinterferenceAbstractBackgroudandbjective:Renalarterystenosiscanbecausedbymanydiseases,themostcommoncausesaremusclefiberdysplasia(FMD)andatherosclerosis.ComparedwithFMD,atherosclerosiscancauserenalfailuermore.Inourcountry,atheroscleroticrenalarterystenosis(ARAS)isthemostcommonprimarydiseaseoftherenalarterystenosis.Studiesinrecentyearshavefoundthatsomeantihypertensivedrugscanloweringbloodpressure,alsohavetheroleofrenalprotection,butthespecificprotectionmechanismisunclear.TherearemanywayscancauserenaldiseasesbyARAS,inwhich,oxidativestressismainpathway.HO-1hasthephysiologialeffectofanti-oxidation,andcanplayanimportantroleintheprotectivefunctionofkidneyfunction.HO-1canbeinducedbymanyfactores.ItisunclearthatwhethertheantihypertensivedrugssuchasdirectrenininhibitorsandcalciumchannelblockerscaninduceHO-1expressedinthekidneyofARAS.Thereisnorelatedreporthomeandabroad.Therefore,weuseoperationmethodtocopyofthesingleandrenalarterystenosisandcombinedhighfatfeedingwithinjecctingVitD3toestablishthemodleofatheroscleroticrenalarterystenosis.BymeasuringthechangeofHO-1andNADPHoxidaseintheleftkidney,toexploretheprotectivefunctionofkidneyanditspossibllymechanismaboutdifferenceantihypertensivedrugs(directrenininhibitorsandcalciumchannelblockers),theproposeistoprovideatheoreticalbasisandstrategiesfortheeffectivetreatmentofrenalarterystenosis.Methods:(1)Animalmodle:36maleSDratswererandomlydividedintoTwoKidneyOneClip,2K1Candcontrolgroup.2K1Cgroupwererenalarterystenosisbyparallelandacupunctureneedlesmethod,thecontrolgroupjustexposedtheleftrenalartery.AlltheratswereinjectedVitD30.5millionIU/kgandhighfatdiettoestablishthemodleofatheroscleroticrenalarterystenosisin10weeks.(2)Studytheprotectivefunctionofkidneyinthemodleofatheroscleroticrenalarterystenosis:After10weeks,theratsofc