简介：AbstractPanax notoginseng is an ancient Chinese medicinal plant that has great clinical value in regulating cardiovascular disease in China. As a single component of panax notoginosides, notoginsenoside R1 (NGR1) belongs to the panaxatriol group. Many reports have demonstrated that NGR1 exerts multiple pharmacological effects in ischemic stroke, myocardial infarction, acute renal injury, and intestinal injury. Here, we outline the available reports on the pharmacological effects of NGR1 in ischemia-reperfusion (I/R) injury. We also discuss the chemistry, composition and molecular mechanism underlying the anti-I/R injury effects of NGR1. NGR1 had significant effects on reducing cerebral infarct size and neurological deficits in cerebral I/R injury, ameliorating the impaired mitochondrial morphology in myocardial I/R injury, decreasing kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin in renal I/R injury and attenuating jejunal mucosal epithelium injury in intestinal I/R injury. The various organ anti-I/R injury effects of NGR1 are mainly through the suppression of oxidative stress, apoptosis, inflammation, endoplasmic reticulum stress and promotion of angiogenesis and neurogenesis. These findings provide a reference basis for future research of NGR1 on I/R injury.

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简介：AbstractMitochondrial injury and endoplasmic reticulum (ER) stress are considered to be the key mechanisms of renal ischemia-reperfusion (I/R) injury. Mitochondria are membrane-bound organelles that form close physical contact with a specific domain of the ER, known as mitochondrial-associated membranes. The close physical contact between them is mainly restrained by ER-mitochondria tethering complexes, which can play an important role in mitochondrial damage, ER stress, lipid homeostasis, and cell death. Several ER-mitochondria tethering complex components are involved in the process of renal I/R injury. A better understanding of the physical and functional interaction between ER and mitochondria is helpful to further clarify the mechanism of renal I/R injury and provide potential therapeutic targets. In this review, we aim to describe the structure of the tethering complex and elucidate its pivotal role in renal I/R injury by summarizing its role in many important mechanisms, such as mitophagy, mitochondrial fission, mitochondrial fusion, apoptosis and necrosis, ER stress, mitochondrial substance transport, and lipid metabolism.

简介：Objective:Toevaluatetheprotectiveeffectsof8%emulsifiedisofluraneaftermyocardialischemia-reperfusioninjuryanditsmechanisminrabbits.Methods:Twenty-fourmaleadultNewZealandwhiterabbitswereanesthetizedwithintravenousinjectionof30mg/kgpentobarbitalfollowedby5mg·kg-1·h-1infusion.Allrabbitsweresubjectedto30minutesofleftanteriorde-scendingcoronaryartery(LAD)occlusionand3hoursofsubsequentreperfusion.BeforeLADocclusion,therabbitswererandomlyallocatedintothreegroupsforprecondi-tioningtreatment(eightforeachgroup).Thecontrolgroup(Cgroup)receivedintravenously0.9%NaClfor30minutes.Theemulsifiedisofluranegroup(EIgroup)received8%emulsifiedisofluraneintravenouslytill0.64%end-tidalcon-centrationfor30minutesthatwasfollowedbya15-minutewashoutperiod.TheIntralipidgroup(INgroup)received30%Intralipidfor30minutes.Theinfarctedarea,plasmamalondialdehyde(MDA)content,superoxidedismutaseactivity(SOD)andnitriteconcentrationafter3-hourmyo-cardialperfusionwererecordedsimultaneously.Results:Forthemyocardialischemia-reperfusionin-juryanimals,theinfarctedsizeintheEIgroupwassignifi-cantlyreduced(91.9%±8%)ascomparedwithcontrolgroup(39%±6%,t=5.19,P<0.01).TheplasmaSODactivityandnitriteconcentrationinEIgroupweresignificantlyhigherthanthoseincontrolgroup(t=2.82,t=8.46,P<0.05),butMDAcontentwaslowerinEIgroupthanthatincontrolgroup(t=2.56,P<0.05).Conclusions:Theresultsindicatethatemulsifiedisofluranehasacardioprotectioneffectagainstischemia-reperfusioninjury.ThisbeneficialeffectofemulsifiedisofluraneisprobablythroughNOreleaseandconsequentlybyincreaseinautioxidationofmyocardium.

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简介：瞄准：为了在ischemia-reperfusion(红外)上调查rosuvastatin的保护的效果，并且在内皮的氮的氧化物synthase(eNOS)的表示上决定这个代理人的效果，在老鼠导致了小肠的损害和发炎蛋白质。方法：肠的损坏被为30min夹钳优异mes伤寒动脉和腹的箱子在男Sprague-Dawley老鼠导致，为60min由灌注列在后面。在生理盐水溶解的Rosuvastatinintraperitoneally被管理在局部缺血前的60min。肠的粘膜损害和发炎的严厉被几个生物化学的标记，以及由组织检查所见评估。eNOS的蛋白质层次被西方的污点决定。结果：当粘膜的索引损坏，管腔内血红素和蛋白质的层次显著地在假冒操作组与那些相比在红外组被增加。然而，这些增加被处理显著地以一种剂量依赖者方式与rosuvastatin禁止。rosuvastatin的保护的效果被组织检查所见也证实。到红外的小肠的暴露导致了thiobarbituric的重要增加描绘的粘膜发炎酸反应的物质，联系织物的myeloperoxidase活动，和老鼠的粘膜内容导致cytokine的嗜中性的chemoattractant-1(CINC-1)和肿瘤坏死factor-alpha(TNF-alpha)。在红外以后的煽动性的参数的这些增加被预告的处理显著地在10mg/kg的剂量与rosuvastatin禁止。而且，CINC-1和TNF-alpha的mRNA表示在红外以后被增加，并且这增加被rosuvastatin也禁止。eNOS的粘膜蛋白质层次在红外期间减少了，但是在与rosuvastatin对待的老鼠被保存。结论：Rosuvastatin禁止老鼠红外导致的肠的损害和发炎，和它的保护与eNOS的保藏被联系蛋白质。

简介：Objective:Toinvestigatenephroprotectiveeffectsofamixtureof8L-aminoacidsonrenalischemia-reperfusioninjuryanditseffectsonrenalendothelin-1(ET-1).Methods:Themixtureof8L-aminoacidsincludesglycine,alanine,threonine,serine,valine,leucine,isoleucineandproline.Acuteischemicrenalinjurywasinducedbyclampingrenalpediclefor45minutesinrats.SixtymaleSprague-Dawieyratswererandomlydividedinto3groups:asham-operatedgroup(GroupA,n=8),acontrolgroup(GroupB,n=26)andanaminoacid-treatedgroup(GroupC,n=26).Aminoacidswereinfusedatarateof1mi·100g-1·h-1Ihourbeforeischemiaandduring3hoursofthewholereperfusion.Theserumcreatininevalues,BUNlevels,creatiulneclearance,urinesodium&potassiumexcretion,urinelactatedehydrogenase(LDH),therateofurineflowandhistologicalexaminationweremeasured.RenalET-1levelswereassayedwithradioimmunologicalassay(RIA)Results:Thecreatinineclearancewas471.0μl/min±121.5pi/maininGroupCand227.0μl/min±27.0μl/mininGroupB3hoursafterreperfnsion,P＜0.01).Theurineflowratewas63.6pi/min±15.2μl/mininGroupCand24.3μl/min±7.7μl/mininGroupB,P＜0.01)1.5hoursafterreperfusion.Theserumcreatininewas85.0μl/min±7.7μmol/LandBUNoncentration11.4mmol/L±3.9mmol/LinGroupCand112.7μmol/L±19.5μmol/Land20.7mmol/L±6.6mmol/LrespectivelyinGroupBafter24hoursofreperfusion(P＜0.05).ThemeanhistologicalscorebystandardsofPallerinkidneyswas108.7±15.7inGroupC,and168.8±14.8inGroupB(P＜0.01).TherenalET-1levels15minuteand3hoursafterreperfusionwere7.2pg/mg±0.8pg/mgand9.6pg/ml±1.0pg/mlinGroupC,and10.1pg/ml±2.8pg/mland13.0pg/ml±2.7pg/miinGroupB(P＜0.01).Conclusions:Themixtureof8L-aminoacidscanprovideremarkableprotectionagainstrenalisehemia-reperfusioninjuryinrats.Thismayassociat

简介：Tostudythechangesofexcitatoryaminoacids(EAAs)andintracellularcalcium([Ca2+]i),andtheprotectiveeffectofEAAsreceptorantagonistsinthetissuesofrabbitlumbarspinalcordafter40-minuesischemiaand4-hoursreperfusion.Methods:Thirtyhealthyrabbitsweredividedintosixgroups:sham-operation,40-minuesischemia,4-hourreperfusion,ketamineandMgSO4treatment,ketaminetreatment,andsalinetreatmentgroups.ThecontentsofEAAs(glutamateandaspartate)and[Ca2+]iweremeasured.Results:Thecontentsofglutamateandaspartateweredecreasedto15.18μmol/g±2.33μmol/gand9.99μmol/g±0.69μmol/g,respectively;13.75μmol/g±2.58μmol/gand6.49μmol/g±1.39umol/gafterreperfusion.Intheischemiagroup,the[Ca2+]iwaselevatedto221.2μg/g±4.27μg/g,andelevatedfurtherto298.3μg/g±9.26μg/gafterreperfusion,beingsignificantlyhigherthanthatofischemiaandcontrolgroups.Ketaminecouldobviouslyincreasethelevelofglutamateandaspartateanddecreasethelevelof[Ca2+]iduringtheischemiaandreperfusioninjury.Conclusions:TheexcitotoxicityofEAAsandtheoverloadofcalciuminducedbyEAAsplayaharmfulroleinischemiaandreperfusioninjury.Ketaminehasaneffectiveinhibitoryeffect.

简介：Inflammationafterstrokeisthemaincauseofcerebralischemia/reperfusioninjury.Cascadingeventsafterinjurycanleadtocelldeath.Heatshockprotein70andotherendogenousinjury-signalingmoleculesarereleasedbydamagedcells,whichcanleadtosystemicstressreactions.Protectingthebrainthroughrepairbeginswiththestress-injury-repairsignalingchain.Thisstudyaimedtoverifywhetheracupunctureactsthroughthischaintofacilitateeffectivetreatmentofischemicstroke.Ratmodelsofcerebralischemia/reperfusioninjurywereestablishedbyZeaLonga'smethod,andinjurysiteswereidentifiedbyassessingneurologicalfunction,2,3,5-triphenyltetrazoliumchloridestaining,andhematoxylin-eosinstaining.ElectroacupunctureatacupointsBaihui(DU20)andZusanli(ST36)wasperformedinthemodelratswithdilatationalwaves,deliveredfor20minutesadayat2–100Hzandanamplitudeof2mA.Weanalyzedthebloodserumfromtheratsandfoundthatinflammatorycytokinesaffectedthelevelsofadrenotrophinandheatshockprotein70,eachofwhichfollowedasimilarbimodalcurve.Specifically,electroacupunctureloweredthepeaklevelsofadrenocorticotrophichormoneandheatshockprotein70.Thus,electroacupuncturewasabletoinhibitexcessivestress,reduceinflammation,andpromotetherepairofneurons,whichfacilitatedhealingofischemicstroke.

简介：BackgroundRecentresearcheshavefoundthatstainscanimproveacutemyocardialischemiareperfusioninjurywhichisachievedbyinhibitinginflammatoryreaction.Xuezhikangisextractedfromredrice,atailor-madeChinesecrudedrug.MaincomponentofXuezhikangthatcaninhibitblood-fatisstatins.MethodsFortyhealthySDrats(halfmaleandhalffemale,200gorso)wererandomlydividedintofourgroups:A:normalcontrol;B:shamoperation;C:MIRgroup;D:Xuezhikanggroup.Theacutemyocardialischemiareperfusioninjurymodelwasproduced.Infarctsizes,MYO,CK-MB,cTnI,IL-10andIL-18weredetectedafterreperfusion.ResultsComparedwithCandDgroup,inAandBgroup,infarctsizewereincreasedsignificantly(P<0.01),thelevelofserumMYO,CK-MB,cTnIwereincreasedsignificantly(P<0.01),thelevelofIL-10weredecreasedsignificantly(P<0.01)andIL-18,CRPwereincreasedsignificantly(P<0.01).ComparedwithCgroup,infarctsizeweredecreasedsignificantly(P<0.05),thelevelofserumMYO,CK-MBandcTnIwereincreasedsignificantly(P<0.05),thelevelofIL-10wereincreasedsignificantly(P<0.05)andIL-18weredecreasedsignificantly(P<0.05).ThelevelofIL-10andIL-18werenodifferencebetweenAandBgroup.ConclusionTheapplicationofXuezhikangcapsulesonratsbeforetheoperationofmyocardialischemiareperfusioncanlesseninflammatoryreactionandreduceinfarctsizesandprotectacutemyocardialischemiareperfusion.

简介：Brainischemicstrokeistheleadingcauseoflong-lastinginjury,disability,anddeathinadults.Althoughthebrainrepresentsonlyabout2%ofthetotalbodymass,itconsumesalmost20%ofthebody’soxygen.Asaresult,braincellsareextremelysensitivetohypoxia.Oncecerebralischemiaoccurs,thecoreofthe

简介：Ephedrinehasaprotectiveeffectagainstcerebralischemia,butitssideeffectslimititsclinicalapplication.Resultsfromapreviousstudyshowedthat1.5mg/kgperdayephedrinecanpromotemotionrecoveryinratsfollowingcerebralischemia/reperfusionwithoutsignificantsideeffects.Inthepresentstudy,ephedrineatdosesof3.0,2.5and2.0mg/kgwasusedtotreatratswithcerebralischemia/reperfusionandtheeffectsofephedrineontheheart,liver,kidneyandcerebrumwereobserved.Resultsshowedthatthebloodpressureofratswithcerebralischemia/reperfusioninjuryfollowingephedrinetreatmentwaslowerthaninratsthatrecoverednaturallyfromcerebralischemia/reperfusion,butthepressuredecreasedwithincreasingdosesofephedrine.Inaddition,serumaspartatetransaminase,alkalinephosphataseandcreatinineconcentrationinratswithcerebralischemia/reperfusioninjuryfollowingephedrinetreatmentweregreaterthaninratsthatrecoverednaturallyfromcerebralischemia/reperfusion.Theconcentrationsoftheseenzymesweredecreasedwithincreasingdosesofephedrine.Ephedrine-treatedratsdisplayedhyperemia,degenerationandedemainthecerebrum,liver,heartandkidney.Resultsdemonstratedthatephedrineexhibitedsideeffectsonthecerebrum,heart,liverandkidneyinratsfollowingcerebralischemia/reperfusioninadose-dependentmanner.

简介：Objective:Toinvestigatetheunderlyingneurobiologicalmechanismoftheprotectiveeffectofelectroacupuncture(EA)duringcerebralischemia-reperfusion(CI-R).Methods:Inthefirstpartofthestudy,15SDratswereevenlyrandomizedintocontrolgroup,CI-R-48hmodelgroupandCI-R-48h+EAgroup.ThecorticalapoptosisandexpressionofBcl-2andBaxproteinsineachgroupweredetectedbyflowcytometer(FCM).Inthesecondpartofthestudy,75SDratswereevenlyrandomizedintocontrol,CI-R-3min,CI-R-3min+EA,CI-R-48handCI-R-48h+EAgroups.Corticalnorepinephrine(NE)concentrationwasdetectedbyfluorescencespectrometer.CI-Rmodelwasestablishedbyocclusionofthebilateralcommoncarotidarteriesandreperfusion.EA(4～16Hz,1～3V)wasappliedafterreperfusionrespectively.Results:Inthefirstpartofthisstudy,resultsindicatedthatthenumberoftheapoptoticneuronsandtheapoptosisrateofCI-R-48hgroupweresignificantlyhigherthanthoseofcontrolgroup;whilecomparisonbetweenCI-R-48h+EAandCI-R-48hgroupsshowedthatthenumberoftheapoptoticneuronsandtheapoptosisrateoftheformergroupweresignificantlylowerthanthoseofthelatergroup(P<0.05).Incomparisonwithcontrolgroup,afterCI-48h,Baxexpressionwasup-regulatedsignificantlyandBcl-2down-regulatedmarkedly(P<0.05).ComparisonbetweenCI-R-48handCI-R-48h+EAgroupindicatedthatBaxexpressionofthelatergroupwassignificantlylowerthanthatoftheformergroup,whileBcl-2expressionofCI-R-48h+EAgroupwassignificantlyhigherthanthatofCI-R-48hgroup(P<0.05),suggestingthatEAcouldreverseCIinducedreactionsofthesetwoindexes.Inthesecondpartofthestudy,incomparisonwithcontrolgroup,NEconcentrationincerebralcortexofCI-R-3mingroupincreasedsignificantly(P<0.05);whileNEcontentofCI-R-3min+EAgroupwassignificantlylowerthanthatofCI-R-3mingroup(P<0.05).NosignificantdifferencewasfoundbetweenCI-R-3mingroupandcontrolgroupincorticalNEl

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简介：NewZealandrabbitswererandomlydividedintoanischemiagroup(occlusionoftheabdominalaortafor60minutes),anischemia-reperfusiongroup(occlusionoftheabdominalaortafor60minutesfollowedby48hoursofreperfusion)andasham-surgerygroup.Two-dimensionalgelelectrophoresisdetected49differentiallyexpressedproteinsinspinalcordtissuefromtheischemiaandischemia/reperfusiongroupsand23ofthemwereidentifiedbymassspectrometry.Intheischemiagroup,theexpressionofeightproteinswasupregulated,andthatoftheremainingfourproteinswasdownregulated.Intheischemia/reperfusiongroup,theexpressionoffourproteinswasupregulated,andthatoftwoproteinswasdownregulated.Inthesham-surgerygroup,onlyoneproteinwasdetected.Intheischemiaandischemia/reperfusiongroups,fourproteinsoverlappedbetweengroupswiththesamedifferentialexpression,includingthreethatwereupregulatedandonedownregulated.Theseproteinswererelatedtoenergymetabolism,celldefense,inflammatorymechanismandcellsignaling.

简介：ToinvestigateeffectsofShenfuinjectionontheconcentrationsofplasmatumornecrosisfactor-alpha(TNF-α)andinterleukin-6(IL-6),activityofNuclearFactorkappaB(NF.gB)andhearttissueultrastructureduringmyocardialischemia/reperfusion(I/R)injuryinratsanditspotentialmechanism.Methods:Myocardialischemia/reperfusion(I/R)wasproducedbyligationandreleaseoftheleftanteriordescendingcoronaryartery.Ischemialastedfor30minandreperfusionfor60min.Twenty-fourhealthymaleSDratsweighing230-280gwererandomlydividedintothreegroups(n=8,each):GroupⅠ(Sham-operationgroup);GroupⅡ(I/Rgroup);GroupⅢ(Shenfugroup),inwhichShenfuinjection(10ml/kg)wasintraperitoneallyinjected30minbeforeischemiainanimalswithI/R.TheplasmaconcentrationsofIL-6andTNF-αweremeasuredbyELISA,andtheheartwasharvestedfordeterminationofNF-κBlevelsbyEcl-westernblotanalysis.Electronmicroscopywasusedtostudyitsultrastructure.Results:Afterreperfusion,NF-κBbindingactivityinmyocardialnucleiandtheplasmaconcentrationsofIL-6andTNF-αweresignificantlyincreasedinGroupⅡ,comparedwithGroupⅠ(P<0.01),andtheyweremarkedlyreducedinGroupⅢ,comparedwithGroupⅡ(P<0.01).Inaddition,electronmicroscopicexaminationshowedmoreseriousinjuryofthemyocardiumultrastructureinGroupⅡ,whileinGroupⅢthemyocardialultrastructurewassimilartonormalstate.Conclusions:ShenfuinjectioninhibitsNF-κBactivityinI/Rmyocardiumandleadstodown-regulationofproinflammatorycytokineexpression,whichmightbeoneofthemolecularmechanismsofShenfuinjectionincardioprotection.

简介：BACKGROUND:RecentstudieshavesuggestedthatmitochondrialATP-sensitiveK+channelopenerscouldreducemyocardiuminfarctsize,andprotectthefunctionofthemitochondria.OBJECTIVE:ToinvestigatethechangesofcerebralinfarctionvolumeandtheactivityofmarkerenzymesinbrainmitochondriaofratsgiventheATP-sensitiveK+channelopener,nicorandil,beforefocalcerebralischemia/reperfusion(I/R).DESIGN,TIMEANDSETTING:Randomized,controlledanimalexperiment,completedattheBrainScientificResearchCenteroftheAffiliatedHospitalofQingdaoUniversityfromJulytoNovember2007.MATERIALS:SixtyhealthymaleWistarratsweighing280–300g.Nicorandil,5-hydroxydecanoate(5-HD)andcytochromeCwerepurchasedfromSigmaintheUSA.Standardmalondialdehyde(MDA)andproteinwerepurchasedfromNanjingJianchengBiotechnologyInstitute.METHODS:Sixtyratswererandomlydividedintoashamoperationgroup,amiddlecerebralarteryocclusion(MCAO)group,anicorandilgroupandanicorandil+5-HDgroup.MCAOfor2hourswasperformedintheMCAOgroup,nicorandilgroupandnicorandil+5-HDgroup.Atotalof5mLsalineweregiventotheMCAOgroupbeforeMCAO.ThenicorandilgroupwasinjectedwiththeATP-sensitiveK+channelopenernicorandil10mg/kgintraperitoneally30minutesbeforeMCAO.Thenicorandil+5-HDgroupwasinjectedwith5-HD10mg/kgintravenously15minutesbeforethesametreatmentasthenicorandilgroup.MAINOUTCOMEMEASURES:Infarctvolumebytotalbrainslicecalculation,activitiesofsuccinatedehydrogenase(SDH)andcytochromeoxidase(CO),andcontentofMDAwereobservedat22hoursofreperfusionafter2hoursMCAO.RESULTS:Sixtyratswereincludedinthefinalanalysis,withoutanyloss.(1)Infarctvolume:comparedwiththeMCAOgroupandnicorandil+5-HDgroup,thepercentageofinfarctvolumewassignificantlydecreasedinthenicorandilgroup(P<0.01).(2)ThecontentofMDA,expressionofSDHandCOinbrain:theexpressionsofSDHandCOintheshamop

简介：Thephenomenonofischemia/reperfusioninjuryisdescribedintheexperimentalmodelsofacutemyocardialinfarction(AMI),causingadditionalfunctionalandstructuraldamagetotheacutereperfusedmyocardium,andischemicpreconditioningreferstothemyocardialischemiaafteralongperiodofreperfusionbeforeoneorseveralshortoccasionalduplicationofmyocardialischemia/reperfusion1,whichcanincreasemyocardialischemictolerance.ThetherapeuticstrategiesforAMIhavefocusedonmyocardialischemia/reperfusioninjury,whichaccountsforasignificantpartofthefinalinfarctsize.Althoughexperimentsinthelast20yearshavereportedthatpharmacologicalinterventionsatreperfusionmightreducemyocardialreperfusioninjury,thiscouldnotbeconfirmedinhumanstudies.Analternativetochemicalmodifiers,postconditioning(briefrepeatedperiodsofischemiaappliedattheonsetofreperfusion)isanothermethodproventobeefficientinanimalmodelsandtobeconfirmedinrecenthumanstudies.Thissimplemethod,appliedinthefirstminuteofreperfusion,reducesthefinalinfarctsizeby30%-50%.Thisreviewwillfocusonthemechanisms,pharmacologicalpreconditioning,postconditioningtechnique,whichiseasilyapplicableinhumanpatientsinthesettingofAMI.

简介：Mitochondriaplayanimportantroleinneuronalapoptosiscausedbycerebralischemia,andtheroleismediatedbytheexpressionofmitochondrialproteins.Thisstudyinvestigatedtheinvolvementofmitochondrialproteinsinhippocampalcellapoptosisaftertransientcerebralischemia-reperfusioninjuryinagedratsusingacomparativeproteomicsstrategy.Ourexperimentalresultsshowthattheagedratbrainissensitivetoischemia-reperfusioninjuryandthattransientischemialedtocellapoptosisinthehippocampusandchangesinmemoryandcognitionofagedrats.Differentialproteomicsanalysissuggestedthatthisphenomenonmaybemediatedbymitochondrialproteinsassociatedwithenergymetabolismandapoptosisinagedrats.Thisstudyprovidespotentialdrugtargetsforthetreatmentoftransientcerebralischemia-reperfusioninjury.

简介：BACKGROUND:Theintegrityofthebloodbrainbarrier(BBB)playsanimportantroleinthepatho-physiologicalprocessofcerebralischemia/reperfusioninjury.Ithasbeenrecentlyobservedthatmetalloproteinase-9(MMP-9)iscloselyrelatedtocerebralischemia/reperfusioninjuryOBJECTIVE:ThisstudywasdesignedtoobserveMMP-9expressionintheratbrainaftercerebralischemia/reperfusioninjuryandtoinvestigateitscorrelationtoBBBpermeability.DESIGN,TIMEANDSETTING:Thisstudy,arandomizedcontrolledanimalexperiment,wasperformedattheInstituteofNeurobiology,CentralSouthUniversitybetweenSeptember2005andMarch2006.MATERIALS:NinetyhealthymaleSDrats,aged3–4months,weighing200–280g,wereusedinthepresentstudy.Rabbitanti-ratMMP-9polyclonalantibody(Boster,Wuhan,China)andEvansblue(Sigma,USA)werealsoused.METHODS:Allratswererandomlydividedinto9groupswith10ratsineachgroup:normalcontrolgroup,sham-operatedgroup,andischemiafor2hoursfollowedbyreperfusionfor3,6,12hours,1,2,4and7daysgroups.Intheischemia/reperfusiongroups,ratsweresubjectedtoischemia/reperfusioninjurybysutureocclusionoftherightmiddlecerebralartery.Inthesham-operatedgroup,ratsweremerelysubjectedtovesseldissociation.Inthenormalcontrolgroup,ratswerenotmodeled.MAINOUTCOMEMEASURES:BBBpermeabilitywasassessedbydeterminingthelevelofeffusionofEvansblue.MMP-9expressionwasdetectedbyanimmunohistochemicalmethod.RESULTS:All90ratswereincludedinthefinalanalysis.BBBpermeabilityalterationwascloselycorrelatedtoischemia/reperfusiontime.BBBpermeabilitybegantoincreaseatischemia/reperfusionfor3hours,thenitgraduallyreachedapeaklevelatischemia/reperfusionfor1day,andthereafteritgraduallydecreased.MMP-9expressionbegantoincreaseatischemia/reperfusionfor3hours,thengraduallyreacheditspeaklevel2daysafterperfusion,andthereafteritgraduallydecreased.CONCLUSION: