简介：ShouwuisatraditionalChinesemedicine(TCM)withneuroprotectiveeffect.ShouwuYizhidecoction(SYD)wasdesignedbasedonTCMtheory.However,littleisknownabouttherolesofSYDinVasculardementia(VaD).ThepresentstudyaimedtoevaluatethepotentialeffectsofSYDonthevascularcognitiveimpairmentandexploretheunderlyingmechanismbyestablishingfocalcerebralischemia/reperfusion(I/R)ratmodeltoinduceVaD.SYDadministration(54mg·kg~(-1))for40daysobviouslyimprovedthevascularcognitiveimpairmentinthemiddlecerebralarteryocclusion(MCAO)ratsasevidencedbythedeclinedneurologicaldeficitscoreandshortenedescapelatencyvianeurologicaldeficitassessmentandMorriswatermazetest.Moreover,SYDdecreasedneurondamage-inducedcelldeathandamelioratedtheultrastructureofendothelialcellsintheMCAOrats,therebyalleviatingVaD.Mechanistically,SYDcausedincreasesintheexpressionofvascularendothelialgrowthfactor(VEGF),CD34andCD31,comparedwiththeMCAOratsincoronalhippocampus.Simultaneously,theexpressionlevelofmiR-210waselevatedsignificantlyafterSYDadministration,comparedwiththevehiclerats(P<0.01).TheexpressionofNotch4atbothmRNAandproteinlevelswasupregulatedremarkablyalongwiththenotablydownregulatedDLL4expressionunderSYDadministrationcomparedwiththevehiclerats(P<0.05).Overall,theaboveresultsindicatedthatSYDpromotedangiogenesisbyupregulatingVEGF-inducedmiR210expressiontoactivateNotchpathway,andfurtheralleviatedneurondamageandamelioratedtheultrastructureofendothelialcellsintheMCAOrats,ultimatelyenhancingthecognitionandmemoryofMCAOrats.Therefore,ourfindingspreliminarilyidentifiedtheeffectandthemechanismofactionforSYDonVaDinrats.SYDcouldbeapotentialcandidateintreatmentofVaD.