简介：然而Wei等[5]在神经元细胞GT1-7中发现Bcl-2中发现Bcl-2可抑制由TG所诱导的凋亡,Yang等[9]与Kluck等[10]发现Bcl-2可以通过抑制线粒体释放Cytc来抑制凋亡,　　Bcl-2抑制细胞凋亡可能与其以下几种作用有关

简介：目的：观察电针天柱穴对大鼠颈椎间盘退变组织bcl-2、bcl—XL表达的影响。方法：将40只SD雄性大鼠，随机分为4组，即假手术组、电针组、西药组和模型组，每组10只。除假手术组外，其余3组造成动静力失衡性颈椎间盘退变模型。电针组给予电针天柱穴、大杼穴治疗；西药组用芬必得治疗；模型组造模后不作任何处理。治疗30d后，运用免疫组化法观察各组大鼠椎间盘组织bcl-2、bcl—xL的表达。结果：bcl-2在电针组、假手术组和西药组中表达明显高于模型组（P〈0．01），电针组、假手术组和西药组之间的表达无显著性差异。bcl-XL在电针组的表达低于假手术组（P〈0．01），高于西药组、模型组（P〈0．01）。结论：电针可以提高大鼠退变椎间盘组织bcl－2、bcl—XL的表达，是其延缓椎间盘组织凋亡，发挥治疗作用的可能途径之一。

简介：Objective:ToinvestigatetheexpressionofE2FandBcl-2andtheclinicopathologicalsignificanceinhepatocellularcarcinoma.Methods:TheexpressionsofE2F-3andBcl-2in74patientswithhepaticcarcinoma,paracarcinomaand15patientswithlivercirrhosisweredetectedbyS-Pimmunohistochemicalstaining.Results:TheexpressionofE2Finhepaticcarcinomawassignificantlyhigherthanthatinparacarcinomaorlivercirrhosis(P<0.005),theexpressionofBcl-2inhepaticcarcinomawassignificantlyhigherthanthatinparacarcinoma(P<0.005),inwhichBcl-2expressionwaslowerthaninlivercirrhosis(P<0.05).TheexpressionofE2F-3wasrelatedwithhistologicalgrade,tumorsize,andtheexpressionofBcl-2wasrelatedwithhistologicalgrade,tumorsizeandtumornumber.TherewascorrelationbetweentheexpressionofE2F-3andBcl-2inhepaticcarcinoma.Conclusion:E2F-3andBcl-2expressionmayplayanimportantroleindevelopment,progressionandcellapoptosisoftumor.

简介：Toinvestigatetheexpressionofapoptosis-relatedprotein(Fas,FasL,andBcl-2)inthepathogenesisofautoimmunethyroiddisorders(ATDs),immunohistochemicalstainingwasperformedon20Hashimoto'sthyroiditis(HT),20Graves'disease(GD),and20thyroidfollicularadenoma(TFA,ascontrol).AllthecasesexpressedFas,mainlyonthecellsurfaceandcytoplasm.FasLwasfoundin17casesoftheTFA.Bcl-2wasdetectedin15casesofHT,19ofGDand17ofTFA.InTFA,amoderateFasexpressionandaminimalornoFasLexpressionwasdetectedonfollicularcells.InHT,thefolliclesadjacenttoinfiltratinglymphocytesshowedincreasedlevelsofFasandFasLexpression.AweakerstainingofFasandFasLwasexhibitedoninfiltratinglymphocytesthanonthyrocytes.InacomparisonofGDwithHT,thyrocytesandlymphocytesshowedsimilarFasstaining,butforFasLthestainingwasratherweakerinHT.TheexpressionofBcl-2wasnearlyidenticalinGDandTFA,butmuchweakeronthefollicularcellsinvicinityoflymphocytesandonthelymphocyteslocatedingerminalcentersofHTtissues.TheexpressionofFas,FasL,Bcl-2inHashimoto'sthyroiditisandGraves'diseasewerealmostsame.FasLstrongexpressionandBcl-2weakexpressiononthefolliclesinHTmayinduceapoptosis.TheseresultsprovidedevidenceforexpressionofFas,FasLandBcl-2inthepathogenesisofautoimmunethyroiddisease.ThelymphocytesseemnottobedirectlyengagedintheprocessviatheirownFasL,buttheymayprovidesomecytokinesthat,inturn,upregulateFasand/orFasLexpressiontoinduceapoptosis.

简介：BCL-2 蛋白家族与细胞凋亡.细胞生物学杂志 2001,Caspase家族与细胞凋亡调控,Caspase家族与细胞凋亡

简介：bcl-2基因是目前已知的抑制细胞凋亡的最重要的一种基因，Bax基因作为bcl-2家庭成员则具有相反的作用，可促进细胞的凋亡。大量的研究表明，凋亡的失控在肿瘤的发生和发展过程中起着重要的作用。本文综述bcl-2基因在乳腺癌、食管癌、胃癌、肝癌、胰腺癌、大肠癌、宫颈癌、卵巢癌和恶性淋巴瘤等研究中的应用。

简介：客观：为了学习表达式和apoptosis的临床的价值，在乳癌控制基因bcl-2和bax。方法：在在1996在我们的医院里从操作获得的41乳癌的蛋白质bax和bcl-2与正常的胸纸巾用ABCimmunohistochemical污点试金并且与10个盒子相比被检测。结果：在正常的胸组织的bax的积极的率是90%并且在乳癌是59%，与他们之间的重要统计差别(P<0.05)，但是在bcl-2没有统计差别蛋白质表示。在41乳癌之中，有淋巴节点转移(21个盒子)的组有显然低的bax表示(43%)和高bcl-2表示(76%)，给没有淋巴节点转移的组显示出重要差别(P<0.05)。结论：bcl-2的antiapoptosis功能是比在乳癌的bax强壮的。蛋白质bax和bcl-2试金可能在理解乳癌的生物行为是有用的。

简介：摘要肿瘤耐药的出现是肿瘤治疗的重大难题。在诸多机制中，肿瘤细胞对凋亡产生抵抗是导致肿瘤耐药的主要原因之一，而抗凋亡基因Bcl-2在肿瘤的凋亡抵抗耐药途径中发挥了重要作用。目前已有研究证实，靶向抑制抗凋亡基因Bcl-2可增加细胞对化疗药物诱导的凋亡，提高疗效。

简介：biflavonoidisochamaejasmin主要在StellerachamaejasmeL的根被散布。(Thymelaeaceae)那在繁体中文药(TCM)被使用治疗肿瘤，肺结核，和干癣。此处，isochamaejasmin被发现对Bcl-2家庭蛋白质显示出类似的bioactivity到参考Bcl-2ligand(−)通过3D类似搜索的-gossypol。它有选择地跳了到Bclx有K和Mcl-1>是的i价值1.93±0.13mol·L−1和9.98±0.21mol·L−1,分别地。另外，isochamaejasmin显示出细微生长对有是的IC50价值的HL-60的禁止的活动50.40±1.21mol·L−1和中等生长对有IC50价值的K562细胞的禁止的活动是24.51±1.62mol·L−1。而且，isochamaejasmin由增加在Bcl-2-inducedapoptosis小径包含了的caspase-9，caspase-3，和PARP的劈开的蛋白质的细胞内部的表示层次导致了K562房间的apoptosis。这些结果显示isochamaejasmin由禁止Bcl-2家庭蛋白质的活动在白血病房间导致apoptosis，提供为进一步学习S的内在的反癌症机制的证据。chamaejasmeL。

简介：摘要B细胞淋巴瘤/白血病-2（Bcelllymphoma/leukemia2，Bcl-2）是一种抗凋亡基因，其在调控线粒体凋亡通路中起着重要作用，与各种乳腺癌的发生、发展、分化、转移、预后及治疗密切相关。Bcl-2与乳腺癌患者中的雌激素受体（ER）、孕激素受体（PR）正相关，与组织分级负相关,bcl-2高表达使乳腺癌的预后更好。通过对Bcl-2的深入研究，能够为乳腺癌的治疗提供新的靶点。

简介：目前已发现数个Bcl-2基因家族成员,主要有Bcl-2、Bax等,它们调节子宫内膜细胞的凋亡,与子宫内膜增生、癌变有密切联系.

简介：Objective:TheexpressionofB-celllymphoma2(Bcl-2)seemstobeinfluencedbytheendocrineenvironment.NumerousreportsdemonstratethediverseexpressionofBcl-2familymembersundersexsteroidregulation.Withtheexceptionofestrogen-relatedtumors,androgen-relatedtumorshaveshowntheircharacteristicsinBcl-2expression.Inthisstudy,thestatusofBcl-2expressioninmalehepatocellularcarcinoma(HCC)patientswasexaminedtoverifythehighincidenceofHCCinmales.Methods:TumortissuemicroarraywasusedtoexamineBcl-2expressionlevelsin374HCCcasesincluding306malesand68females.Kaplan-Meiermethod,log-ranktest,andCoxproportionalhazardsmodelwereappliedtoinvestigatethepredictivevalueofBcl-2inHCCpatients.Results:ImmunohistochemistryanalysisshowedthatmalepatientswithhigherBcl-2levelshadsignificantlylongermediansurvivaltimeandrecurrencetimethanthosewithlowerlevels.However,nosignificantdifferencesinoutcomeswerefoundbetweendifferentBcl-2levelsinfemalepatients.Whenthemalepatientswerestratifiedintoseveralagepoints,thelevelofBcl-2expressionshowedpoorerpredictiveefficiencyinthe45–49and55–60agegroupsinandropause-agepatientscomparedwithotheragegroups.Bcl-2wasanindependentprognosticfactorforbothoverallsurvival(P<0.0001)andrecurrencetime(P=0.0001)inmalepatients.Afterexcludingmalepatientsinthe45–60agegroup,thepredictiveefficiencywasenhanced(n=147,OS,P=0.0002,TTR,P<0.0001).Conclusions:Bcl-2expressionisanindependentpredictorofsurvivalandrecurrenceinmaleHCC.Bcl-2levelsmayalsoberegulatedbyandrogensorandrogenreceptorsinmaleHCCpatients.Bcl-2levelschangeandexhibitpoorpredictiveefficiencywhenandrogenlevelsvarydramatically(andropauseage).

简介：Objective:Toinvestigatetheeffectoftwoantisenseoligonucleotidesoncellsurviving,bcl-2expressionandapoptosisofleukemiacells.Methods:Theexperimentalassayswereperformedwithcellculture,immunochemistryandflowcytometry.Results:Thetwoantisenseoligodeoxynucleotides,combinedwithVp16orAra-corDNR,wereabletodeclinethesurvivalrateofmyeleukemiccells,downregulatebcl-2geneexpressionandinduceapoptosisofleukemiccellssignificantly,ascomparedwithVp16orAra-corDNRalone.Conclusion:Itispossibleforthetwonewbcl-2antisensestobedevelopedintoclinicaltrialsforleukemiaandtumorwithbcl-2geneoverexpression.

简介：Objective:TostudythedifferencesandsimilaritiesoftheantisensedrugswithdifferentstructuresonthebiologicalfunctionsofK562cells.Methods:Cytotoxiceffectsweremeasuredbyuseofacellviabilityassay.FlowcytometricanalysisandagarosegelelectrophoresisofDNAfragmentationwerealsoperformed.Theexpressionlevelofproteinwasassayedbyimmunofluorescenceusingfluoresceisothiocyanatelabel.Results:PNAtargetingthecodingregionoftheBcl-2messengerRNAcouldeffectivelyinhibitK562cellviability,down-regulatethesynthesisoftheBcl-2proteinandincreasecellapoptosis.By72haftertheBcl-2antisensePNAtreatment,K562cellsshowedmorereductioninthelevelofBcl-2proteincomparedwithcellstreatedwiththeantisenseODN.Aftertreatmentwith10μmol/LofBcl-2antisensePNAorantisenseODNfor72h,apoptoticratesofK562cellswere13.15±1.13and11.72±1.12,respectively.Furthermore,therewassignificantdifferenceinthepercentageofapoptoticcellsbetweenantisensePNAgroupandantisenseODNgroup.Conclusion:TheresultssuggestthatantisensePNAtargetingthecodingregionofBcl-2mRNAhasbetterantisenseeffectsthantheantisenseoligonucleotidesoninducingapoptosisofK562cells.

简介：Objective:TostudytheexpressionofFasandBcl-2proteinsonTlymphocytesubsetsintheperipheralbloodofrelapsingpatientswithcondylomaacuminatum(CA)andhealthycontrols.Methods:Flowcytometry(permeabizationandstainingprocedurewithconjugatedantibodies)wasused.Results:WeobservedthattheexpressionofFasproteinonCD4^+TlymphocytesubsetofCApatientswassignificantlyhigherthanthatofhealthycontrols(P<0.01).Conclusions:IncreasedexpressionofFasproteinonCD4^+Tlymphocytesubsetmaybeacauseofde-creasedpercentageofCD4^+Tlymphocytesubset.ThisinducestheincreasedratioofCD4^+/CD8^+.

简介：肿瘤进展与治疗失效的一个显著标志就是凋亡抵抗。经常可以在复发的前列腺癌中检测到抗凋亡蛋白Bcl-2的过表达并增加了激素治疗与化疗的难度。然而，Bcl-2的拮抗剂-ABT-737在前列腺癌细胞并未显现出其促凋亡的活性。

简介：Minimalresidualdisease(MRD)playsacausativeroleintumorrecurrenceandestablishmentofeffectiveandsensitiveassessmentofMRDcouldbeveryusefulforstagingandevaluationoftreatmentofdisease.Inthisstudy,weassessedtheusefulnessofhcf-2/JHPCRanalysisonoccultlymphoma...

简介：目的：测定胃黏膜病变组织PCNA、BCL-2和BAX的表达，探讨其在胃黏膜病变过程中的变化规律和所起的作用。方法：用免疫组化染色法检测88例经胃镜和病理确诊的不同胃黏膜病变患者的病变组织中PCNA、BCL-2和BAX的表达，探讨它们之间的关系及变化规律。结果：PCNA从浅表性胃炎→萎缩性胃炎→肠腺化生→异型增生→胃癌中的表达逐渐增强，BCL-2在胃癌中的表达最高，而BAX的表达与BCL-2相反，在浅表性胃炎中表达最强，经相关性分析PCNA与BAX成负相关（r=-0．320，P〈0．01），与BCL-2成正相关（r=-0．430，P〈0．01）。结论：胃黏膜病变从浅表性胃炎→萎缩性胃炎→肠腺化生→异型增生→胃癌的变化过程中，PCNA、BCL-2和BAX表达的异常在其中发挥重要作用。

简介：

简介：MitochondrialK+-ATP(mito-KATP)channelsplayanimportantroleincellularfunctionandsurvivalfollowingischemicstress.Thepresentresultsrevealedthatinterventionwithdiazoxide,amito-KATPchannelopener,ledtoanincreaseinBcl-2expressioninthecerebralcortexofratssubjectedtocerebralischemiareperfusioninjury.Inaddition,theinterventionalsoledtoclearimprovementsinneuronalmitochondrialmorphologyandconsciousnesspost-injury.Glibenclamide,amito-KATPchannelblocker,exhibitedtheconverseeffects.Bothdiazoxideandglibenclamideexerteddose-dependenteffects(inparticular,at18mg/kgdiazoxideand25mg/kgglibenclamide).Thesefindingssuggestthatdiazoxideexertsaneuroprotectiveeffectoncerebralischemiareperfusioninjurybyopeningmito-KATPchannelsandupregulatingBcl-2expression.