简介：ObjectivesToevaluatetheimpactofstentimplantationonproliferationandapop-tosisininjuredmediavascularsmoothmusclecells(VSMC)andtoexplorethemechanismofrestenosisafterstentimplantation.MethodsFiftymaleNewZealandrabbitswererandomizedintotwogroups,includingballoongroupandstentgroup.Controlgroupwassetup.Thesampleswereharvestedon3,7,14,28,56daysafteroperationandthefollowinginvestigationwascarriedout:(1)Assessingtheexpressionofproliferatingcellnuclearantigen(PCNA)ofmediaVSMCbythemethodofimmunohistochemistry;(2)AnalyzingapoptosisofmediaVSMCbyDNAagarosegelelectrophoresisandTUNELtechnique.ResultsTheexpressionofPCNAandapoptosisinstentandballoongroupsweremarkedlyincreasedcomparedwithcontrolgroups.(1)StentgroupinducedsignificantincreasedexpressionofPCNAinthemediaVSMCcomparedwithballoongroupon3to28days.Onday7,thepositiveratesofPCNAwere24.36±0.55%vs18.74±1.09%

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简介：Thepanaxnotoginsengsaponin(PNS)hadbeenclinicallyusedforthetreatmentofcardiovasculardiseasesandstrokeinChina.IthadbeendemonstratedthatPNScouldprotectcardiomyocytesfrominjuryinducedbyischemi-a,buttheunderlyingmolecularmechanismsofthisprotectiveeffectwerestillunclear.ThisstudywasaimedtoinvestigatetheprotectiveeffectandmolecularmechanismsofPNSonapoptosisinH9c2cellsinvitroandratmyocardialischemiainjurymodelinvivo.Annexin-V/PIassayshewthatPNScouldprotectH9c2cellsfromapoptosisinducedbyserum,glucoseandoxygendeprivation(SGOD)inadose-dependentmanner.However,theanti-apoptoticeffectofPNSwasreversedbyLY294002,aspecificPI3Kinhibitor.ThisantiapoptoticeffectofPNSwasconfirmedbyJC-1,aspecificprobeofmitochondrialmembranepotentialstaining.PNScouldsignificantlyincreasephos-AktinH9c2cellsbyWesternblotassaysanditseffectcouldbeinhibitedbyLY294002.Furthermore,PNScouldimproveischemic-inducedleftventricularfunctionasreflectedbyEF,LVDdandLVDs.PNScouldalsoinhibitedcellularapoptosisinmyocardialtissuesinischemicratsbyTUNELassay.PNSadministrationalsoincreasedtheexpressionofphos-Aktinratischemicmyocardialtissues.TheseresultssuggestedthatPNScouldprotectmyocardialcellsfromapoptosisinducedbyischemiainvitromodelandinvivomodelthroughactivating-PI3K/AktsignalpathwaywhichmaybemeaningfulforfurtherunderstandingthemolecularmechanismsofcardiacprotectionofPNS.Andtheresultsmightbeusefulintreatmentofmyocardialischemiainfuture.