简介：AbstractObjective:Clinically, low-dose aspirin and progesterone are frequently used to prevent pregnancy loss. We investigated the effect of these drugs on the biological behavior of human extravillous trophoblasts in vitro.Methods:HTR-8/SVneo cells were cultured in vitro and treated with different concentrations of aspirin and progesterone. The proliferation, invasion, and apoptosis of HTR-8/SVneo cells were assessed using a cell counting Kit-8 assay, Matrigel Transwell assay, and Hoechst staining, respectively. Reverse transcriptase polymerase chain reaction was used to verify the expression of related genes. Reactive oxygen species (ROS) levels were detected using the 2,7-dichlorofluorescin diacetate assay.Results:Low-dose aspirin alone, progesterone alone, or aspirin plus progesterone upregulated the proliferation and invasion and decreased the apoptosis of HTR-8/SVneo cells. Moreover, the expression of marker of proliferation Ki-67 (MKI67), matrix metalloproteinases 2 (MMP2), and MMP9 was increased. In addition, low-dose aspirin plus progesterone exerted stronger anti-apoptosis effects than low-dose aspirin and progesterone alone. Interestingly, aspirin upregulated the expression of progesterone receptor (PGR). Treatment with hydrogen peroxide (H2O2) promoted ROS production in HTR-8/SVneo cells; however, low-dose aspirin plus progesterone significantly restricted H2O2-mediated ROS production and apoptosis in HTR-8/SVneo cells.Conclusions:These data suggest that low-dose aspirin and progesterone promote proliferation and invasion and cooperatively reduce oxidative stress and apoptosis in trophoblasts in vitro. These results may provide an experimental basis for the combined application of aspirin and progesterone to prevent unexplained recurrent spontaneous miscarriage, especially in patients with trophoblast dysfunction.

简介：AIM:ToinvestigatetheeffectofhepatitisBvirus(HBV)XgeneonapoptosisandexpressionsofapoptosisfactorsinXgene-transfectedHepG2cells.METHODS:TheHBVXgeneeukaryonexpressionvectorpcDNVA3-XwastransientlytransfectedintoHepG2cellsbylipid-mediatransfection.UntransfectedHepG2andHepG2transfectedwithpcDNA3wereusedascontrols.ExpressionofHBxinHepG2wasidentifiedbyPT-PCR.MTTandTUNELwereemployedtomeasureproliferationandapoptosisofcellsin.threegroups.Semi-quantifiedRT-PCRwasusedtoevaluatetheexpressionlevelsofFas/FasL,Bax/Bcl-xL,andc-mycineachgroup.RESULTS:HBVXgenewastransfectedintoHepG2cellssuccessfully.RT-PCRshowedthatHBxwasonlyexpressedinHepG2/pcDNA3-Xcells,butnotexpressedinHepG2andHepG2/pcDNA3cells.AnalyzedbyMTT,cellproliferationcapacitywasobviouslylowerinHepG2/pcDNA3-Xcells(0.08910±0.003164)thaninHepG2(0.14410±0.004927)andHepG2/pcDNA3cells(0.12150±0.007159)(P＜0.05andP＜0.01).AnalyzedbyTUNEL,cellapoptosiswasmuchmoreinHepG2/pcDNA3-Xcells(980/2000)thanHepG2(420/2000),HepG2/pcDNA3cells(520/2000)(P＜0.05andP＜0.01).Evaluatedbysemi-quantifiedRT-PCR,theexpressionlevelofFas/FasLwassignificantlyhigherinHepG2cellstransfectedwithHBxthaninHepG2andHepG2/pcDNA3cells(P＜0.05andP＜0.01).Bax/Bcl-xLexpressionlevelwasalsoelevatedinHepG2/pcDNA3-Xcells(P＜0.05andP＜0.01).Expressionofc-mycwasmarkedlyhigherinHepG2/pcDNA3-XcellsthaninHepG2andHepG2/pcDNA3cells(P＜0.05andP＜0.01).CONCLUSION:HBVXgenecanimpaircellproliferationcapacity,improvecellapoptosis,andupregulateexpressionofapoptosisfactors.TheinterventionofHBVXgeneontheexpressionofapoptosisfactorsmaybeapossiblemechanismresponsibleforthechangeincellapoptosisandproliferation.

简介：AbstractObjective:To detect the expression of caspase-3, baculoviral inhibitor of apoptosis repeat containing 5 (BIRC-5), vascular endothelial growth factor (VEGF), hypoxia-inducible factor (HIF), and the concentration of resistin protein in placental of patients with gestational diabetes mellitus (GDM) and normal pregnant women, and to explore its correlation with the pathogenesis of GDM and its significance.Methods:This study includes 30 pregnant women who chose cesarean section at Tongji Hospital of Tongji Medical College during May 2013 to February 2014: 15 GDM patients and 15 normal glucose tolerance patients, 26-36 years old. The expression of caspase-3, VEGF, HIF, and BIRC-5 in placenta of 15 patients with GDM (GDM group) and 15 normal late pregnancy (control group) was detected by real-time fluorescence quantitative polymerase chain reaction. The concentration of resistin protein in the placenta was detected by enzyme-linked immunosorbent assay.Results:Compared with the control group, the expression of caspase-3, HIF, VEGF, resistin in placenta of GDM group increased significantly (P < 0.05); the expression of BIRC-5 in placenta of GDM group decreased significantly (P < 0.05).Conclusion:The expression of caspase-3, BIRC-5, VEGF, HIF, and resistin in placenta of GDM patients and normal pregnant women are significantly different, which may be involved in the pathogenesis of GDM disease.

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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%

简介：AIMTo在氢过氧化物上探索parthenolide的效果(H2在人的透镜的O2)-inducedapoptosis上皮(HLE)apoptoticHLE房间的cells.METHODSThe形态学和数字用光被估计显微镜学和流动cytometry。房间生存能力被山试金测试。另外，相关蛋白质的表示被HLE房间的西方的污点assay.RESULTSApoptosis测量被200导致??丠?????あψ

简介：Thevisualsystemisvitaltohumanhealth,andtheeffectsofionizingradiationonvisionhavereceivedincreasingattention.Usingazebrafishmodel,thisstudywasdesignedtoinvestigatetheapoptosisineyesinducedbycarbonionirradiation.Zebrafishembryosat12hpost-fertilization(hpf)wereirradiatedusing12C6+ionbeamsatdosesof2,4and8Gy.

简介：ObjectiveToinvestigatetheoccurrenceandpossiblemechanismsofapoptosisincochlearepitheliumandspiralganglionneuronsaftermefloquinetreatment.MethodsWeusedquantitativeRT-PCRapoptosis-focusedgenearrays(96-well,84apoptosisrelatedgenes)toassesschangesofgeneexpressioninthecochlearbasilarmembrane(haircells-supportingcells)andspiralganglionneuronsofratcochlearorganotypicculturestreatedwith100μMmefloquinefor3h.ResultsSignificantup-ordown-regulationingeneexpressionwasdetectedin23genesinthecochlearbasilarmembrane,andin32genesinthespiralganglionneuronscomparedwithtime-matchedcontrols.Therespondinggenescouldbeclassifiedaspro-oranti-apoptotic,andweremainlyimplicatedintheBcl-2,Caspase,Card,IAP,TNFligand/TNFreceptor,Deathdomain/Deatheffectordomain,DNAdamage/p53,andNF-kappaBfamilies.Syntheticanalysissuggestedthatthesefamiliescouldberevisedtotwomajorpathwaysmainlyinvolvedinthedeathreceptor-mediatedsignalingpathwayandapoptoticmitochondrialpathway.Inaddition,itwasfoundthatnumerousanti-apoptoticgenessuchasBcl2a1,Birc1b,Birc3,Birc4,Bnip1,Cflar,Il10,Lhx4,Mcl1,Nfkb1,Prlr,Prok2,andTNFweregreatlyup-regulatedinthecochleartissue,whichmightimplytheco-existenceofprotectiveresponseinthecellsattheearlystageofmefloquine-induceddamage.

简介：Objective:TumorassociatedantigenencodinggeneHCA520(AF146019)wasidentifiedbyscreeningahumanhepatocellularcarcinomaexpressingcDNAlibraryusingSEREXtechnique.InthisexperimentwestudiedtheeffectofHCA520oncellproliferationandapoptosis.Methods:GeneHCA520wasgainedbyPCRandtransfectedinto293cells.ThestableexpressioncellswereobtainedbyG418selection.Thecellproliferationwasmeasuredby[3H]-TdRuptakeandapoptosisassaywasmeasuredbyFACS.Results:EukaryoticexpressionplasmidpcDNA3-HCA520wasconstructedanditsstabletransfectantswereobtained.OverexpressionofHCA520inhibitedthecellproliferationandenhancedcellapoptosisafterserumdeprivation.Conclusion:HCA520isanoveltumorassociatedantigenthatcanaffectcellproliferationandapoptosis.

简介：瞄准：在正常检测易碎的组氨酸三个一组(FHIT)的表示，并且分析它的关系，织物CRC，和联系apoptosis的蛋白质展示clinicopathological渲染表面的织物，渲染表面的腺瘤并且渲染表面的癌症(CRC)(Bcl-2，Bax，survivin)并且在颜色的apoptosis表面的癌症。方法：FHITmRNA分析被嵌套的反向的抄写聚合酶执行链反应(RT-PCR)试金。织物微数组(TMA)被建立在80个CRC织物标本检测FHIT，Bcl-2，Bax和survivin基因的表示，16在象控制的时间的一样的时期期间渲染表面的腺瘤织物标本和16个痔(PPH)织物标本。Citrate-microwave-SP被用作免疫组织化学的方法。在clinicopathological因素之间的关系，例如区别，等级和5年的幸存率被观察。TUNEL试金被用来在80个CRC织物标本检测apoptosis索引。结果：十(38.5%)从26，CRC织物标本表示了异常FHIT抄本，任何一个都没在匹配的正常织物异常FHIT抄本被观察并且由嵌套的RT-PCR渲染表面的腺瘤织物试金。在正常的FHIT基因表示的积极的率渲染表面的织物，渲染表面的腺瘤和癌织物分别地是93.75%，68.75%和46.25%。病人的Clinicopathological分析证明减少的FHIT基因表示没与年龄，性别，浆液CEA层次，肿瘤地点和尺寸被联系，组织学的分类。然而，FHIT的表示与等级，病理学的阶段，淋巴节点转移和5年的幸存在操作以后评估的区别被相关。在CRC织物的联系apoptosis的蛋白质(Bax，Bcl-2和survivin)的积极的率分别地是72.50%，51.25%和77.50%。在CRC织物的这些联系apoptosis的蛋白质的表示与FHIT的表示被相关。在FHIT否定肿瘤的吝啬的apoptosis索引在FHIT积极肿瘤是比那显著地低的(5.41+/-0.23对0.56+/-0.10，P<0.01)。结论：FHIT基因在apoptosis的规定起一个重要作用，减少的FHIT表示在肤色的开始和前进起一�

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：Ｔ－ＬＹＭＰＨＯＣＹＴＥＭＥＤＩＡＴＥＤＴＵＭＯＲＣＥＬＬＤＥＳＴＲＵＣＴＩＯＮＩＮＶＩＶＯＡＳＳＯＣＩＡＴＩＮＧＷＩＴＨＡＳＰＥＣＩＦＩＣＦＥＡＴＵＲＥ　ＯＦ　ＡＰＯＰＴＯＳＩＳＹｕＤａ鱼达；ＹａｎｇＨｕａ杨骅；ＺｈｅｎｇＳｈｕ郑树；ＷａｎｇＸｉａ...

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：Recentstudiesindicatethatcell-cyclecheckpointsaretightlycorrelatedwiththeregulationofapoptosis,inwhichp53playsanimportantrole.OurpresentworksshowthattheexpressionofE6/E7oncogenesofhumanpapillomavirusinHeLacellsisinhibitedinthepresenceofanti-tumorreagenttripchlorolide(TC),whichresultsintheup-regulationofp53inHeLacells.Interestingly,underthesameTC-treatment,thecellsattheearlyS-phasearemoresusceptibletoapoptosisthanthoseatthemiddleS-phasealthoughp53proteinisstabilizedtothesamelevelinbothsituations.Significantdifferenceisexhibitedbetweenthetwospecifiedexpressionprofiles.Furtheranalysisdemonstratesthatanti-apoptoticgenesurvivinisup-regulatedbyp53intheTC-treatedmiddle-Scells,whereasitisdown-regulatedbyp53intheTC-treatedearly-Scells.Takentogether,thepresentstudyindicatesthatthedifferentialp53-regulatedexpressionofsurvivinatdifferentstagesofthecellcycleresultsindifferentcellularoutputsunderthesameapoptosis-inducer.

简介：Toevaluatetheeffectofadenovirus-mediatedp53gene(Adp53)onapoptosisandradiosensitivityofhumangastriccarcinomacelllines.Methods:Recombinantadenovirusexpressingwild-typep53lineswithdifferentp53geneticstatus.p53proteinexpressionwasdetectedbyimmunohistochemistryassayandwesternblotassay.Cellsurvivalwasassessedusingaclonogenicassay.TUNELassaywasusedindeterminationofapoptosis.FourhumangastriccarcinomacellsinfectedwithAdp53wereirradiatedwith4GyandcellcycledistributionandSub-G1peakwereassayedbyflowcytometry.Results:G2/Marrest,apoptosisandinhibitionoftumorcellproliferationwereinducedbyinfectionatAdp53at100MOIwhichcausedhightransferrateofwild-typep53andstrongexpressionofp53proteininfourhumangastriccarcinomacells.Theradio-enhancementratioofAdp53at4Gywere3.0forWcell,3.6forMcell,2.2forneocelland2.5for823cellinvitro.Conclusion:ThisstudydemonstratedthatAdp53transferincreasedcellularapoptosisandradiosensitivityofhumangastriccarcinomacelllinesinvitroindependentlyoncellularintrinsicp53statusthussupportingthecombinationofp53genetherapywithradiotherapyinclinicaltrials.

简介：在apoptotic小径以内的缺点在前列腺癌症(PCa)被含有tumorigenesis，变形前进和治疗抵抗。癌症的一个特点是出轨的能力由禁止apoptotic信号，减少apoptotic蛋白质的表达式或放大幸存的apoptosis通过antiapoptotic的增加的生产发信号分子。这评论描述在热吃惊蛋白质(HSP)和人的雄激素之间的协会受体(AR)，HSP的角色和在PCa开发的另外的导致压力的蛋白质和在指向这些保护的蛋白质对待PCa的新兴的策略。

简介：人的免疫不全病毒类型1(HIV-1)Vpr导致房间死亡在哺乳动物并且分裂酵母房间，建议那Vpr可以影响一个保存细胞的过程。然而，导致Vpr的酵母房间死亡是否在哺乳动物的房间模仿调停Vpr的apoptosis，是不清楚的。我们最近识别了很多Vprsuppressors不仅在分裂酵母压制导致Vpr的房间死亡，而且在哺乳动物的房间堵住导致Vpr的apoptosis。这些调查结果建议在酵母的导致Vpr的房间死亡可以类似于一些哺乳动物的房间的apoptotic过程。这研究的目标是为apoptosis的未来研究开发并且验证一个分裂酵母模型系统。类似于在哺乳动物的房间的导致Vpr的apoptosis，我们这里证明在分裂酵母的Vpr支持phosphatidylserine外表表现并且导致线粒体的hyperpolarization，导致mitochondrial膜潜力的变化。而且，反应的氧种类(ROS)的Vpr扳机生产，显示象apoptotic一样细胞死亡可能被ROS调停。有趣地，Vpr在可以为在分裂酵母测量象apoptotic一样过程提供一个简单标记的线粒体导致唯一的词法变化。验证这可能性，我们测试了二Vprsuppressors(EF2和Hsp16)除了最新识别的Vprsuppressor(Skp1)在哺乳动物的房间压制导致Vpr的apoptosis。所有三蛋白质废除了房间死亡由Vpr调停了并且在酵母房间恢复了正常mitochondrial形态学。在结论，在分裂酵母的导致Vpr的房间死亡类似于哺乳动物的apoptotic过程。分裂酵母可以潜在地因此为Vpr和另外的proapoptotic代理人导致的象apoptotic一样过程的未来学习被用作一个简单模型有机体。

简介：BACKGROUND:Studieshavedemonstratedthatthemechanismsunderlyingcellularapoptosissignaltransductionfocusontwopathways:intracellularmitochondriaandextracellulardeathreceptor.Thecurrentevidencesupportsthatsignaltransductionofcellularapoptosisalsoincludesendoplasmicreticulumstresssignaltransduction.OBJECTIVE:ToobserveCaspase-12expressionandcellularapoptosisfollowingischemiainratswithprogressivespinalcordcompression,andtoverifytheinfluenceofendoplasmicreticulumstressontheapoptosisinducedbyspinalcordinjury.DESIGN,TIMEANDSETTING:Arandomized,controlled,animaltrialwasperformedattheInstituteofNeuroscienceinChongqingMedicalUniversitybetweenJanuaryandOctoberin2006.MATERIALS:Immunohistochemicalkit,diaminobenzidine,andTUNELkitwerepurchasedfromBeijingZhongshanBiotechnology,China;rabbitanti-ratCaspase-12monoclonalantibodywasprovidedbySantaCruz,USA.METHODS:SixtyWistarrats,aged3-4months,wererandomlyassignedtoamodelgroup(n=50),whichunderwentspinalcordcompressionintheL_1segmentfollowingL_1laminectomyandarticularprocessexcisiontoestablishamodelofprogressivespinalcordcompression,andasham-surgerygroup(n=10),whichunderwentonlylaminectomy.Startingwiththefirstdayaftersurgery,theratswerelocallyanesthetized,theskinwasopened,andthescrewwasrotatedby1/4ofacycle,twiceweekly.MAINOUTCOMEMEASURES:At3,7,14,21,and28daysaftersurgery,ratsfromeachgroupwereanesthetized,andthespinalcordswereresected.Pathologicalchangesfollowingspinalcordcompressionweredeterminedusinghematoxylin-eosinstaining,Nissldye,andtransmissionelectronmicroscopy.TheTUNELmethodwasusedtoobserveneuronalapoptosisinthecompressedspinalcordsegments.ImmunohistochemistryandWesternblotwereutilizedtodetectCaspase-12expressioninthecompressedsegments.RESULTS:Cellularswelling,neuraldegeneration,andalteredendoplasmicreticulumstructureswereobservedat3days

简介：Toobservetheeffectsofdifferentacupuncturemanipulationsonbloodpressureandtargetorgandamageinspontaneouslyhypertensiverats(SHRs),thisstudyusedthereinforcingtwirlingmethod(1.5–2-mmdepth;rotatingneedleclockwisefor360°andthencounterclockwisefor360°,withthethumbmovingheavilyforwardandgentlybackward,60timesperminutefor1minute,andretainingneedlefor9minutes),thereducingtwirlingmethod(1.5–2-mmdepth;rotatingneedlecounterclockwisefor360°andthenclockwisefor360°,withthethumbmovingheavilybackwardandgentlyforward,60timesperminutefor1minute,andretainingneedlefor9minutes),andtheneedleretainingmethod(1.5–2-mmdepthandretainingtheneedlefor10minutes).BilateralTaichong(LR3)wastreatedbyacupunctureusingdifferentmanipulationsandmanualstimulation.Reinforcingtwirling,reducingtwirling,andneedleretainingresultedinadecreasednumberofapoptoticcells,reducedBaxmRNAandproteinexpression,andanincreasedBcl-2/BaxratiointhehippocampuscomparedwiththeSHRgroup.Amongthesegroups,theBcl-2/Baxproteinratiowashighestinthereducingtwirlinggroup,andtheBcl-2/BaxmRNAratiowashighestintheneedleretaininggroup.Theseresultssuggestthatreinforcingtwirling,reducingtwirling,andneedleretainingmethodsallimprovebloodpressureandpreventtargetorgandamagebyincreasingthehippocampalBcl-2/BaxratioandinhibitingcellapoptosisinthehippocampusinSHR.

简介：Formationofapoptoticbodiesisatypicalcharacterofapoptoticcelldeath,buthowtheprocessesarecontrolledisnotknown.Inthisstudy,wecomparedtwoapoptosisinducingsystemsinvascularendothelialcells(VEC).Wefoundthattheformationofapoptoticbodiesduringapoptosisinducedbyrattlesnakevenom,whichisanuniqueandspecificapoptosisinducertovascularendothelialcells,wasmuchfasterthanthatinducedbydeprivationofsurvivalfactors(aFGFandserum).WhenweblockedthesynthesisofmRNAsincellstreatedwithrattlesnakevenombyDRB(5,6-dichloro-1-β-D-ribofuranosylbenzimidazole),aninhibitoroftranscription,theformationofapoptoticbodieswasdramaticallyinhibited.WeexaminedtheexpressionofP^53geneandfoundthatitsexpressionwasmuchhigherinapoptosisinducedbyrattlesnakevenomthatthatinapoptosisinducedbydeprivationofaFGFandserum.OurresultssuggestthatgeneexpressionisimportantandP^53genemayplayamajorroleininducingtheformationofapoptoticbodiesinVEC.