红景天苷对大鼠脑缺血再灌注损伤的保护作用

红景天苷对大鼠脑缺血再灌注损伤的保护作用

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页数:42页

时间:2019-02-19

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1、———————————————型必芏趔f兰li垫塞ProtectiveEffectandItsMechanismofSalidrosideagainstCerebralIschemia·ReperfusionInjuryinRatsAbstraetAstheadvancementofthemechanismaboutcerebralischemia—reperfusioninjury.newphysiopathologicmechanismhasbeenrecognizedAlotofinvestigati

2、onshavebeenconfirmedthatreperfusionafteracutefocalcerebralischemiacarlaggravatetheinjuryAtpresent,themostextensivelyanddeeplystudiedaspectsarefreeradicleinjuryandtheexpressionoftheproteinassociatedwithapoptosisRecently,salidrosidewhichisthemaineffectiveing

3、redientofintegripetalrhodiolaherbhasbeenreportedpossessingextensivepharmacologicalactionsThemaineffectsofsalidrosideareenhancingmemory,protectingcardiovascularsystem,enhancingimmunity,resistinghypoxiaandsoonMorestudieshavebeenfocusedontheprotectiveeffectof

4、salidrosideagainstcardiovasculardisease,however,theneuroprotecdveeffectofsalidrosideespeciallyinvivowaslessstudiedThepurposesofthepreseatstudyv/ergtoevaluatetheeffectsofsalidrosideonfreeradicatscavengerandtheproteinexpressionassociatedwithapoptosisinMCAOra

5、tsPartIOBJECTIVEToinvestigatetheeffectsofsalidrosideoncerebralischemia-reperfusioninjuryinmiddlecerebralarteryocclusive(MCAO)ratsMETHODSFocalcerebralischemiainratswasproducedby15hocclusionofthemiddlecerebralarteryand24hreperfusionSalidroslde(25、5、10mg’kg“)

6、wasadministeredintravenouslyimmediatelyafterocclusionandreperfusionrespectivelyTheneurologicdeficitscorewasinvestigatedaccordingtoZea-LongalsStandardTheinfarctareawasassessedwithsoftwareImageproPlus60afterTTCstainingRESULTSComparedwiththemodelgroupsalidros

7、ide(5、10mg/kg)cansignificantlydecreasetheneurologicdeficitscoreandreducetheinfarctareaofthebraininMCAO—I/RratsCONCLUSIONSalidrosidecouldprotectMCAOratsfromcerebralischemia—reperfusioninjuryPartIIOBJECTIVEToexploretheeffectsofsalidrosideonactivitiesofGSH—PX

8、andiNOSaswellastheexpressionofapoptosisrelatedproteininMCAO-I/RratsMETHODSSDratssvererandomlydividedintoshamgroup,modelgroupandsalidroside5mg/kggroupTheactivitiesofinduciblenitricoxidesynthase(iNOS)andglutath

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