简介：Objective:Toobservehumanneuronalapoptosissecondarytotraumaticbraininjury,andtoelucidateitsregulativemechanismandthechangeofexpressionofapoptosis-relatedgenes.Methods:Specimensofbrainwerecollectedfromcasesoftraumaticbraininjuryinhumans.Thehistologicalandcellularmorphologywasexaminedbylightandelectronmicroscopy.TheextentofDNAinjurytocorticalneuronswasdetectedbyusingTUNEL.ByinsituhybridisationandimmunohistochemistrythemRNAchangesandproteinexpressionofBcl-2,Bax,p53,andcaspase3p20subunitwereobserved.Results:Apoptoticneuronsappearedfollowingtraumaticbraininjury,peakedat24hoursandlastedfor7days.Innormalbraintissueactivatedcaspase3wasrare,butashorttimeaftertraumaitbecameactivated.Theactivitypeakedat20-28hoursandremainedhigherthannormalfor5-7days.TherewasnoexpressionofBcl-2mRNAandBcl-2proteininnormalbraintissuebut8hoursafterinjurytheirexpressionbecameevidentandthenincreased,peakedat2-3daysandremainedhigherthannormalfor5-7days.TheprimaryexpressionofBax-mRNAandBaxproteinwashighinnormalbraintissue.At20-28hourstheyincreasedandremainedhighfor2-3days;onthe7thdaystheyreturnedtoanormallevel.Innormalbraintissue,p53mRNAandP53wereminimallyexpressed.Increasedexpressionwasdetectedatthe8thhour,anddecreasedat20-28hoursbutstillremainedhigherthannormalonthe5thday.Conclusions:Followingtraumaticinjurytothehumanbrain,apoptoticneuronsappeararoundthefocusoftrauma.ThemRNAandproteinexpressionofBcl-2,Baxandp53andtheactivityofcaspase3enzymeareincreased.

简介：Objective:Toexploretherelationshipbetweenneuronalapoptosisandhypoxiaortraumaticinjury.Methods:Ratneuronsprimarilyculturedinvitroweretreatedwithhypoxia(thehypoxiagroup)ortraumaticinjury(thetraumagroup).Theneuronalapoptosiswasevaluatedwithmicroscope,TUNEL(terminaldeoxynucleotidyltransferasemediatedx-dUTPnickendlabeling)staining,flowcytometry,agarosegetelectrophoresisandimmunohistochemistry.Results:Morphologicalchangesofapoptosisappearedinthetreatedneurons,andtheDNAfragmentationshowed“ladder”break.Theapoptoticindexwas10.8%inthehypoxiagroupand4.8%inthetraumagroup,whileitwasonly1.6%inthecontrolgroup.Theexpressionofapoptosis-associatedgenes(c-myc,fasandfasL)increased.Conclusions:Hypoxiaortraumaticinjurycaninduceneuronalapoptosis,anditsmolecularmechanismisprobablyrelatedtotheexpressionsofapoptosis-associatedgenes.

简介：Objective:Tostudythecorrelationbetweenbrainedema,elevatedintracranialpressure(ICP)andcellapoptosisintraumaticbraininjury(TBI).Methods:Inthisstudy,totally42rabbitsin7groupswerestudied.Sixoftheanimalswereidentifiedasacontrolgroup,andtheremaining36animalswereequallydividedinto6TBIgroups.TBImodelswereproducedbythemodifiedmethodofFeeney.Aftertheimpact,ICPofeachsubjectwasrecordedcontinuouslybyanICPmonitoruntiltheanimalwassacrificedatscheduledtime.Theapoptoticbraincellsweredetectedbyanterminaldeoxynucleotide-transferase-mediateddUTP-digoxigeninnickendlabeling(TUNEL)assay.Cerebralwatercontent(CWC)wasmeasuredwithadryingmethodandcalculatedaccordingtotheElliottformula.Then,ananalysiswasconductedtodeterminethecorrelationbetweenthecountofapoptoticcellsandtheclinicalpathologicalchangesofthebrain.Results:Apoptoticcellcountbegantoincrease2haftertheimpact,andreacheditsmaximumabout3daysaftertheimpact.ThepeakvalueofCWCandICPappeared1dayand3daysaftertheimpact,respectively.ApoptoticcellcounthadapositivecorrelationwithCWCandICP.Conclusions:InTBI,occurrenceofbrainedemaandICPincreasemightleadtoapoptosisofbraincells.Anytherapywhichcanrelievebrainedemaand/ordecreaseICPwouldbeabletoreduceneuronapoptosis,therebytoattenuatethesecondarybraindamage.

简介：Toexplorethemolecularmechanismoftheprotectiveeffectofnervegrowthfactor(NGF)oninjuredspinalcord.Methods:TheposteriorT8(the8ththoracicsegment)spinalcordsof60Wistarratswereinjuredbyimpactscausedbyobjects(weighing10g)fallingfromaheightof2.5cmwithAllensway.Solutionwithnervegrowthfactors(NGF)wasgivento30rats(theNGFgroup)throughamicrotubuleinsertedintothesubarachnoidcavityimmediately,andat2,4,8,12and24hoursafterspinalcordinjury(SCI)respectively.Normalsaline(NS)withsamevolumewasgiventotheother30rats(theNSgroup)withthesamemethod.And5normalratsweretakenasthenormalcontrols.Theexpressionofbcl-2andbaxproteinsinspinalcordwasdetectedwithimmunohistochemistry.Theapoptoticneuronsinspinalcordweremeasuredwithterminaldeoxynucleotidyltransferase-mediateddUTP-biotinnickend-labelingofDNAfragments(TUNEL)staining.Results:Thepositiveexpressionofbcl-2proteinwasstronginthenormalcontrols,butdecreasedintheNSgroup,andincreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).Thepositiveexpressionofbaxproteinwasalsostronginthenormalcontrols,butincreasedintheNSgroup,anddecreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).ApoptoticneuronswerefoundintheNSgroup,andtheydecreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).Conclusions:NGFcanprotecttheinjurednervetissuesthroughstimulatingtheexpressionofbcl-2protein,inhibitingtheexpressionofbaxproteinandinhibitingtheneuronalapoptosisafterSCI.

简介：Objective:　Toexplorethevariantprocessesofcellapoptosisandtheinhibitingeffectofmoderatehypothermiaoncellapoptosisafterdiffusebraininjury.　　Methods:　ModelsofdiffusebraininjurywereinducedbythetraumadevicereportedbyMarmarou.1Atotalof128Wistarratsweredividedinto4groups:theuninjuredgroup(GroupA,n=8),theseverelyinjuredgroup(GroupB,n=60),themildlyinjuredgroup(GroupC,n=30)andthemildhypothermiagroup(GroupD,n=30).InGroupD,theseverelyinjuredratsweretreatedwithmoderatehypothermiatokeeptherectaltemperatureat32℃(standarddeviationfor0.1℃)for6hours.Thenthemorphosis,thecharacteristicsandthequantityofapoptoticcellsinthecerebralcortexandinthehippocampusregionsafterdifferentseveritiesofcraniocerebralinjurieswereobservedandcomparedunderanelectronicmicroscope,withterminaldeoxynucleotidylnickendlabeling(TUNEL)inDNAfragmentationandwithagarosegelelectrophoresis.　　Results:　TUNELshowedapoptoticcellsincreasedaccordingtotheinjuryseverity,andtheypeakedat48hoursafterinjuryandthendeclined.InGroupC,apoptosiswaslocatedintheCA2andCA3areasofthehippocampus.AndinGroupB,apoptosisincreasedevidently,andlocatedinthewholehippocampusandinthefrontalandparietalcortexregions.Thehypothermia-treatedratshadsomeapoptoticcells,too.However,evenat24,48and72hoursafterinjurythereweresignificantlyfewerapoptoticcellsinthecortexandinthehippocampusinGroupDthanthatinthenon-treatedgroups.Electronmicroscopyshowedthattheapoptoticcellswereroundandshrunkeninmorphologyandthenucleiwereroundandcondensedat24and48hoursafterinjury.Andtheapoptosisat48hourswasmoreseverethanthatat24hours.Thehypothermia-treatedratshadnoapoptoticcells.GelelectrophoresisshowedthatcharacteristicDNA“ladders”wereobservedinthecortexandinthehippocampusat48hoursafters

简介：Aim:ToobservetheapoptoticchangesfollowingexposuretoEMPandtoexplorethepossibleinjurymechanisminNIH-3T3fibroblasts.Methods:FollowingNIH-3T3cellswereexposedtoEMP,theproliferationandviabilityofNIH-3T3fibroblastswereestimatedbyhemacytometerandMTTMeasurements.Apoptoticratewasmeasuredbyflowcytometer.TheimnmohistochemicalSPmethodwasusedtodeterminebcl-2,p53.ThepositivelystainedcellswereanalyzedwithCMIAS-Ⅱimageanalysissystematamagnification400.AlldatawereanalyzedbySPSS8.0software.Results:TheproliferationandviabilityofNIH-3T3cellsweremarkedlyinhibitedandsignificantapoptosiswasinducedfollowingexposuretoEMP.EMPcouldincreasethenumberofnon-adherentcells,thehighestratio(33.9%)ofnon-adherentcellsalsooccurredat6h.TheAs70valueofMTTdecreasedimmediatelyat1h,6hfollowingthecellswereexposedascomparedwiththecontrol(P＜0.05).Thehighestratioofapoptosiswas15.07%at6h,thendecreasedgradually.Down-regulationofbcl-2andup-regulationofp53wereinducedbyEMP(P＜0.05).Conclusions:EMPcouldpromoteapoptosisofNIH-3T3fibroblasts.EMPcouldalsodown-regulatebcl-2levelandup-regulatep53levelinNIH-3T3fibroblasts.Bcl-2andp53genemaytakepartintheprocessofapoptosis.

简介：客观：在兔子在针的绳索ischemia/reperfusion(I/R)以后在lipidperoxidation和apoptosis上学习白果树biloba摘录(GBE)的效果。方法：SpinalcordI/R损害模型根据对Erten等的描述被建立。27只NewZealand白兔子的一个总数随机被划分成三个组：一个假冒的组(9只兔子对待withs火腿操作但是没有大动脉的吸藏)，一个模型组(与大动脉的吸藏对待的9只兔子并且匹配卷盐)，并且一个GBE组(与大动脉的吸藏andGinaton(100mg/kg)对待的9只兔子在大动脉的夹钳前并且在灌注的发作注射了30分钟)。Theneurological结果分别地在灌注以后在24和48个小时被评估。针的绳索malondialdehyde(MDA)水平，超级氧化物dismutase(草皮)然后被检测。神经cellapoptosis被终端deoxynucleotidyltransferase(TdT)决定标记的-mediateddUTP-fluorescence刻痕结束(TUNEL)方法和bcl-2和bax的表示是examinedhistologically在有免疫组织化学的针的绳索。结果：I/Rproduced在神经病学的得分的重要减少。GBE组的马达分数比在在灌注以后的24和48个小时的模型组的那些显著地高(P<0.05)。与模型组相比，GBE改善了草皮的下面规定并且生产了MDA水平的重要减小(P<0.01)。为在模型组的TUNEL的积极房间是多于GBE组的那些的大部分(P<0.01)。bcl-2在I/R以后是起来调整的，特别在theGBE组(P<0.01)。bax的起来规定被GBE极大地减少(P<0.01).Conclusions：GBE对针的绳索I/R损害，和机制有保护的效果可以是它能清除氧释放激进分子并且禁止神经房间的apoptosis。

简介：Objective:TostudytherelationshipbetweentheexpressionofBax,Bcl-2proteins,andapoptosisinradiationcompoundwoundhealingofrats.Methods:Apoptosis,BaxandBcl-2proteinswereestimatedbyinsituterminallabeling(TUNEL)andimmunohistochemicalmethods.Results:(1)Changesoftheapoptosisinwoundhealingshowedthreetypicalcharacteristics:earlyoccurrence,highfrequencyanddelayeddisappearanceafterradiationtoratswhencomparedwiththoseofsimplewoundgroup,whichmightbeanimportantreasonforradiation-induceddelayedwoundhealing.(2)TheexpressionofBaxproteinincreasedevidentlywiththeincrementofapoptosisandshowedagoodcorrespondingrelationshipwiththeapoptoticfrequencyintheprocessofwoundhealing.WhiletheexpressionofBcl-2proteindecreasedobviouslyastheapoptosisreachedamaximumandshowedincreasingtendencyuptonormallevelwhentheapoptosisdecreaseddistinctively.Conclusions:BaxandBcl-2proteinsplayanimportantroleintheapoptoticregulationofradiationcompoundwoundhealinginrats.