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.

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简介：AbstractBackground:Sweat secreted by eccrine sweat glands is transported to the skin surface through the lumen. The eccrine sweat gland develops from the initial solid bud to the final gland structure with a lumen, but how the lumen is formed and the mechanism of lumen formation have not yet been fully elucidated. This study aimed to investigate the mechanism of lumen formation of eccrine gland organoids (EGOs).Methods:Human eccrine sweat glands were isolated from the skin for tissue culture, and the primary cultured cells were collected and cultured in Matrigel for 14 days in vitro. EGOs at different development days were collected for hematoxylin and eosin (H&E) staining to observe morphological changes and for immunofluorescence staining of proliferation marker Ki67, cellular motility marker filamentous actin (F-actin), and autophagy marker LC3B. Western blotting was used to detect the expression of Ki67, F-actin, and LC3B. Moreover, apoptosis was detected using a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) apoptosis assay kit, and the expression of poly (ADP-ribose) polymerase and Caspase-3 was detected by Western blot. In addition, 3-methyladenine (3MA) was used as an autophagy inhibitor to detect whether the formation of sweat glands can be effectively inhibited.Results:The results showed that a single gland cell proliferated rapidly and formed EGOs on day 4. The earliest lumen formation was observed on day 6. From day 8 to day 14, the rate of lumen formation in EGOs increased significantly. The immunofluorescence and Western blot analyses showed that the expression of Ki67 gradually decreased with the increase in days, while the F-actin expression level did not change. Notably, the expression of autophagy marker LC3B was detected in the interior cells of EGOs as the apoptosis signal of EGOs was negative. Compared with the control group, the autophagy inhibitor 3MA can effectively limit the formation rate of the lumen and reduce the inner diameter of EGOs.Conclusion:Using our model of eccrine gland 3D-reconstruction in Matrigel, we determined that autophagy rather than apoptosis plays a role in the lumen formation of EGOs.

简介：Ahallmarkofallformsofneurodegenerativediseasesisimpairmentofneuronalfunctions,andinmanycasesneuronalcelldeath.Althoughtheetiologyofneurodegenerativediseasesmaybedistinct,differentdiseasesdisplayasimilarpathogenesis,forexampleabnormalimmunitywithinthecentralnervoussystem(CNS),activationofmacrophage/microgliaandtheinvolvementofproinflammatorycytokines.Recentstudiesshowthatneuronsinaneurodegenerativestateundergoahighlyregulatedprogrammedcelldeath,alsocalledapoptosis.TNF-relatedapoptosis-inducingligand(TRAIL),amemberoftheTNFfamily,hasbeenshowntobeinvolvedinapoptosisduringmanydiseases.Asonememberofadeathligandfamily,TRAILwasoriginallythoughttotargetonlytumorcellsandwasnotpresentinCNS.However,recentdatashowedthatTRAILwasunregulatedinHIV-1-infectedandimmune-activatedmacrophages,amajordiseaseinducingcellduringHIV-1-associateddementia(HAD).TRAILisalsoinducedonneuronbyβ-amyloidprotein,animportantpathogenforAlzheimer'sdisease.Inthisreview,wesummarizethepossiblecommonaspectsthatTRAILinvolvedthoseneurodegenerativediseases,TRAILinducedapoptosissignalingintheCNScells,andspecificroleofTRAILinindividualdiseases.Cellular&MolecularImmunology.2005;2(2):113-122.

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简介：肿瘤坏死因素相关的导致apoptosisligand(小道)是为anticancer的一个有希望的代理人治疗。能建立前列腺癌症(PCa)的敏感的小分子的鉴定房间到导致小道的apoptosis为PCa的指向的治疗是关键的。PC3，DU145，JAC-1，TsuPr1，和LNCaP房间与Andrographolide(Andro)被对待，小道，和apoptosis用AnnexinV/PI被测量两倍染色的方法。真实时间聚合酶链反应(PCR)和西方的污点分析被执行测量目标分子的表示层次。RNA干扰技术习惯于下面调整目标蛋白质的表示。我们建立了PCa的一个裸体老鼠异种皮移植模特儿，它被用来用流动cytometry在肿瘤房间测量caspase-3活动。在这研究研究，我们的结果证明Andro优先地在subtoxic集中增加了PCa房间的敏感到导致小道的apoptosis，并且规定机制与DR4的起来规定有关。另外，它也增加了p53表示并且在细胞导致了反应的氧种类(ROS)的产生。进一步的研究表明DR4抑制，p53表示，和ROS产生罐头显著地减少小道和Andro的联合在PCa房间导致的apoptosis。在结论，Andro通过ROS的产生和p53的起来规定增加PCa房间的敏感到导致小道的apoptosis然后支持与DR4的激活联系的PCa房间apoptosis。

简介：Manystudiesdemonstratethatconventionalanticancerdrugselevateintracellularlevelofreactiveoxygenspecies(ROS)andalterredox-homeostasisofcancercells.ItiswidelyacceptedthatanticancereffectofthesechemotherapeuticsisduetoinductionofoxidativestressandROS-mediatedapoptosisincancer.Ontheotherhand,theharmfulsideeffectsofconventionalanticancerchemotherapyarealsoduetoincreasedproductionofROSanddisruptionofredox-homeostasisofnormalcellsandtissues.ThisarticledescribesthemechanismsfortriggeringandmodulationofapoptosisthroughROS-dependentandROS-independentpathways.Wetrytoanswerthequestion:'Isitpossibletoinducehighlyspecificapoptosisonlyincancercells,withoutoverproductionofROS,aswellaswithoutharmfuleffectsonnormalcellsandtissues?'Thereviewalsosuggestsanewtherapeuticstrategyforselectivekillingofcancercells,withoutsignificantimpactonviabilityofnormalcellsandtissues,bycombininganticancerdrugswithredox-modulators,affectingspecificsignalingpathwaysandavoidingoxidativestress.

简介：有建议激活的apoptosis在呼喊的人的精子发信号否定地影响他们的授精潜力的证据的基本身体。然而，发信号的这apoptotic是否是与精子发生有关的未成功的apoptosis的一件遗物，仍然是争论的或如果它应该在导致stereotypical的成熟精子被认为是一条功能的preformed小径词法变化思考原子拆卸。探讨这个问题，apoptosis在密度坡度centrifugation充实的成熟、不成熟的呼喊的人的精子用betulinic酸被导致。apoptosis的执行被经由传播电子显微镜学观察极端词法的变化监视。在体的房间的apoptosis的典型词法符号与apoptotic身体，损害mitochondrial正直，原子信封的缺点，和原子破碎的形成包括血浆膜blebbing；这些形态学也在人的精子被观察了。另外，这些apoptotic特征在与成熟精子相比的不成熟的精子是更经常的。后面的betulinic酸处理，apoptosis相关的词法变化从健康施主在成熟精子被导致。这效果更不在不成熟的精子被读。而且在两部分，betulinic酸处理增加了反应acrosome的精子的百分比。我们的极端词法的学习的结果在成熟呼喊的人的精子证明apoptosis的功能的胜任。一个唯一的未成功的过程的理论可能为不成熟的精子仅仅是有效的。由刺激apoptosis的acrosome反应的正式就职可能使精子apoptosis的生物关联清楚些。

简介：AbstractCell death occurs in various tissues and organs in the body. It is a physiological or pathological process that has different effects. It is of great significance in maintaining the morphological function of cells and clearing abnormal cells. Pyroptosis, apoptosis, and necrosis are all modes of cell death that have been studied extensively by many experts and scholars, including studies on their effects on the liver, kidney, the heart, other organs, and even the whole body. The heart, as the most important organ of the body, should be a particular focus. This review summarizes the mechanisms underlying the various cell death modes and the relationship between the various mechanisms and heart diseases. The current research status for heart therapy is discussed from the perspective of pathogenesis.

简介：调查apoptosis的表示的目的联系了基因p53；在乳房的管的不正常的增生的bcl-2；在基因表示之间的关系；胸的瘤形成。apoptosis的方法mRNA联系了基因p53；bcl-2被原位杂交在不正常的管的增生的44种情况中检测。p53蛋白质表示被免疫组织化学检测。数据与良性的增生的6个案例的那些相比；胸癌的26个案例。结果p53mRNA的表示在良性的增生是66.7%，40%在不正常的管的增生(55.6%在里面温和，41.7%在媒介，26.1%在里面严重)；19.2%在癌(哪个21.4%是管内的癌；16.7%是侵略的)。p53蛋白质的表示在良性的增生是否定的，24%在不正常的增生(温和11.1%，媒介25%，严重34.8%)，38.5%在癌(管内癌35.7%，侵略管的癌41.7%)。bcl-2的表示在良性的增生是否定的，78.6%在管内癌，83.3%在侵略管的癌。结论损失；p53基因的变化；过多的表示bcl-2mRNA在严重不正常的管的增生被检测。

简介：AIM:Toexploretheeffectsandmechanismofvascularendothelialcadherin(VE-cadherin)onexperimentalcornealneovascularization(CRNV).·METHODS:MousecorneaswereburnedwithsodiumhydroxidetobuildaCRNVmodel.Theburnedcorneaswerelocallyadministratedwithanti-mouseVE-cadherinneutralizingantibody.AnnexinVandclusterofdifferentiation31(CD31)doublestainingwasusedtomeasurevascularendothelialcellapoptosiswiththeuseofflowcytometry(FCM).TheproteinexpressionofNADPHoxidase2(Nox2),caspase-3,andproteinkinaseC(PKC)intheburnedcorneaswereexaminedbyWesternblot.Humanretinalendothelialcell(HREC)proliferationwasdetectedusingaCellCountingKit8(CCK-8)assayinvitro.·RESULTS:TheamountofCRNVpeakedtwoweeksafterthealkaliburn.FCMconfirmedthatVE-cadherinneutralizingantibodytreatmentincreasedCD31positivecellapoptosis.WesternblotrevealedthattheintracornealproteinexpressionofNox2andcaspase-3wereup-regulated,whilePKCwasdown-regulatedintheVE-cadherinneutralizingantibodyadministratedgroup.CCK-8assayshowedthatVE-cadherinneutralizingantibodymarkedlyinhibitedHRECproliferation.·CONCLUSION:VE-cadherinexhibitedananti-apoptosiseffectthroughenhancedPKCsignalingandanenhancedcellproliferationpathway.

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简介：ＡＰＯＰＴＯＳＩＳＯＦＴＵＭＯＲＣＥＬＬＳＩＮＬＥＣＴＩＮ－ＤＥＰＥＮＤＥＮＴＬＹＭＰＨＯＫＩＮＥ－ＡＣＴＩＶＡＴＥＤＫＩＬＬＥＲＣＥＬＬＭＥＤＩＡＴＥＤＣＹＴＯＴＯＸＩＣＩＴＹＤｏｎｇＨａｉｄｏｎｇ董海东；ＸｉｎｇＲｏｎｇ邢嵘；ＧｕｏＬｉａｎｙｉｎ...

简介：AIM:Toevaluatetheroleofsurvivinandcaspase-3inapoptosisofgastriccarcinoma,aswellasinprognosisofpatientswithgastriccarcinoma.METHODS:Expressionsofsurvivinandcaspase-3wereinvestigatedimmunohistochemicallyin80gastriccarcinomapatientswithoutahistoryofchemo-radiationtherapy.TumorcellapoptosiswasexaminedbyTUNELmethod.RESULTS:Immunohistochemicalanalysisshowedthatsurvivinexpressionwaspositivein61of80patients(76%)withgastriccarcinoma.Incontrast,noexpressionofsurvivininadjacentnormaltissueswasdetected.Expressionlevelofcaspase-3washigherinnormaltissuesthanincarcinoma.Patientswithhigherexpressionofsurvivinhadworsehistologicalgradesandpathologicalstages.Expressionofcaspase-3wassignificantlyassociatedwithhistologicalstages,butnotwiththepathologicalstages.Althoughsurvivinexpressionincarcinomawasnotinverselyrelatedtocaspase-3,patientswithsurvivin(-)andcaspase-3(+)hadthemaximumapoptosisindex.CONCLUSION:Expressionlevelofsurvivinwasassociatedwithhistologicalgradesandpathologicalstagesofthetumor,indicatingthatsurvivinmaybeapoorprognosisfactorforgastriccarcinoma.Unlikecaspase-3,survivin(anapoptosisinhibitor)canmarkedlyinhibittheapoptosisoftumorcells.

简介：Aim:Tostudytheapoptoticrate(AR)andtheandrogenandestrogenmilieuintheproximalanddistalductalsystemsofprostate,inordertohelpexploringtheeffectsofthesefactorsonprostaticgrowthandthepathogenesisofbenignprostatichypertrophy(BPH).Methods:Theproximalanddistalendsoftheductalsystemwereincisedfrom20normalprostateaswellasthehypertrophicprostatetissuefrom20patientswithBPH.TheARwasdeterminedbytheDNAend-labelingmethodanddihydrotestosterone(DHT)andestrodiol(E2),byradioimmunoassay.Results:TherewasnosignificantdifferenceinDHTandE2densitybetweentheproximalanddistalendsoftheductalsystemsinnormalprostate.E2appearedtobehigherinBPHthaninnormalprostatictissues,butthedifferencewasstatisticallyinsignificant.Innormalprostatictissue,theARwassignificantlyhigherinthedistalthanintheproximalendsoftheductalsystem(P＜0.05),whiletheARoftheproximalendswassignificantlyhigher(P＜0.01)thanthatintheBPHtissue.NosignificantcorrelationwasnotedbetweentheDHTandE2densityandtheARbothinthenormalprostateandBPHtissues.Conclusion:ThepaperisthefirsttimedescribingadifferenceinARindifferentregionsoftheductalsystemofnormalprostate,whilethehormonalmilieuissimilar,indicatingafunctionalinhomogeneityoftheseregions.AlowARintheproximalduct,whereBPHoriginates,andanevenlowerARintheBPHtissue,suggestingtheparticipationofapoptosisintheBPHpathogenesis.

简介：ObjectiveTheaimofthisstudyistoinvestigatetheeffectoftransfectedhTERTgeneoncellapoptosisofnewbornratcochlearbasilarmembranecells(CBMCs).MethodsCBMCsisolatedfromnewbornratcochlearweretransfectedusingaplasmidcontaininghumantelomerasereverasetranscriptasegene(pCI-neo-hTERT),andwerescreenedusingG418toobtainstabletransfectedcelllines.Cellapoptosisratewasanalyzedbyflowcytometry.hTERTandapoptosisrelatedgenesexpressionweredetectedbyreversetranscriptasepolymerasechainreaction(RT-PCR).ResultshTERTgeneexpressionwasdetected72hoursaftergenetransfectionintransfectedcells.TheapoptoticrateoftransfectedCBMCssignificantlyreduced.Expressionofapoptosisrelatedgenescorrespondinglychanged.ConclusionTransfectionofhTERTgeneleadstoreducedapoptosisrateinnewbornratCBMCs.andlowerexpressionofapaf1,Caspase3andBCL2intransfectedcellsascomparedtothatofnormalCBMCs.

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：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.