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500 个结果
  • 简介:瞄准:与ulcerative(UC)在病人的结肠的粘膜检验metalloproteinase-1(MMP-1)和metalloproteinase-1(TIMP-1)的织物禁止者的表示。方法:颠倒抄写聚合酶链反应(RT-PCR),免疫组织化学被用来与UC和控制在病人在mRNA和蛋白质层次学习MMP-1和TIMP-1的表达式。在MMP-1mRNA,TIMP-1mRNA,MMP-1mRNA/TIMP-1mRNA比率和有UC的病人的临床的症状的严厉之间的关系也被分析。结果:MMP-1mRNA和TIMP-1mRNA在的表示溃烂并且煽动了结肠的粘膜在非煽动的结肠的粘膜比那显著地高(P<0.001),但是有不,统计上,在UC病人和正常的非煽动的结肠的粘膜的有效差量控制(P>0.05)。在UC病人的溃烂的结肠的粘膜的MMP-1和TIMP-1的mRNA表达式被80褶层和2.2褶层增加,分别地什么时候与正常控制相比。在煽动的结肠的粘膜,增加分别地是30褶层和1.6褶层。Immunohistochemical分析显示出那在之中溃烂,发炎,并且UC病人的非煽动的结肠的mucosae和正常控制,MMP-1表示的积极的率分别地是87%,87%,40%和35%,并且TIMP-1表示的积极的率分别地是89%,89%,80%和75%。而且,MMP-1mRNA,TIMP-1mRNA和MMP-1mRNA/TIMP-1mRNA比率的表示与临床的症状(P<0.05)的严厉被相关。结论:在结肠的粘膜在UC病人引起细胞外的矩阵(ECM)和溃疡的过多的水解作用的diseased的MMP-1的过多的表示。MMP-1mRNA,TIMP-1mRNA和MMP-1mRNA/TIMP-1mRNA比率能被用作简历标记与UC在病人判定临床的症状的严厉。外长的TIMP-1或MMP-1禁止者治疗是为有UC的病人的新奇治疗。

  • 标签: 基因表达 大肠炎 溃疡疾病 治疗
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  • 简介:Objective:Oxidativestressislinkedtoincreasedriskofgastriccancerandmatrixmetalloproteinases(MMPs)areimportantintheinvasionandmetastasisofgastriccancer.WeaimedtoanalyzetheeffectoftheaccumulationofoxidativestressinthegastriccancerMKN-45and23132/87cellsfollowinghydrogenperoxide(H2O2)exposureontheexpressionpatternsofMMP-1,MMP-3,MMP-7,MMP-9,MMP-10,MMP-11,MMP-12,MMP-14,MMP-15,MMP-17,MMP-23,MMP-28,andβ-cateningenes.Methods:ThemRNAtranscriptsinthecellsweredeterminedbyRT-PCR.FollowingH2O2exposure,oxidativestressintheviablecellswasanalyzedby2’,7’-dichlorofluoresceindiacetate(DCFH-DA).Caffeicacidphenethylester(CAPE)wasusedtoeliminateoxidativestressandtheconsequenceofH2O2exposureanditsremovalontheexpressionsofthegeneswereevaluatedbyquantitativereal-timePCR.Results:TheexpressionsofMMP-1,MMP-7,MMP-14,MMP-15,MMP-17andβ-catenininMKN-45cellsandonlytheexpressionofMMP-15in23132/87cellswereincreased.RemovaloftheoxidativestressresultedindecreaseintheexpressionsofMMPgenesofwhichtheexpressionswereincreasedafterH2O2exposure.β-catenin,atranscriptionfactorformanygenesincludingMMPs,alsodisplayeddecreasedlevelsofexpressioninbothofthecelllinesfollowingCAPEtreatment.Conclusions:OurdatasuggestthatthereisaremarkablelinkbetweentheaccumulationofoxidativestressandtheincreasedexpressionsofMMPgenesinthegastriccancercellsandMMPsshouldbeconsideredaspotentialtargetsoftherapyingastriccancersduetoitscontinuousexposuretooxidativestress.

  • 标签: 基质金属蛋白酶 氧化应激 胃癌细胞 蛋白酶基因 细胞株 MMP-14
  • 简介:Objective:Toobservetheinfluenceofintra-articularinjectionofsodiumhyaluronate(HA)onthemRNAexpressionsofmatrixmetalloproteinase-1,-3(MMP-1,-3)andtissueinhibitorofmetalloproteinase-1(TIMP-1)incartilageandsynoviumoftraumaticosteoarthritis(OA).Methods:Sixteenwhiterabbitsunderwentunilateralanteriorcruciateligamenttransection(ACLT)weredividedinto2groupsrandomly5weeksaftertransection.Theexperimentalgrouprabbitsreceived0.3mlof1%HAbyintra-articularinjectiononceaweek.Animalsinthecontrolgroupweretreatedunderthesameconditionsusingphysiologicalsaline.Tenweeksfollowingsurgery,cartilageandsynoviumwereharvested.ThemRNAexpressionsofMMP-1,MMP-3andTIMP-1wereanalyzedusingreversetranscription-polymerasechainreaction(RT-PCR).Results:Insynovium,themRNAexpressionofMMP-3wassuppressedintheHAinjectiongroup.HAtreatmenthadnoeffectontheMMP-3expressionincartilage.NosignificantdifferenceofMMP-1andTIMP-1expressionsincartilageandsynoviumwasfoundbetweentheHAinjectiongroupandthecontrolgroup.Conclusions:OneofthemechanismsofthetherapeuticeffectofHAmaybetheinhibitionofexpressionofMMP-3insynoviumduringearlystageoftraumaticOA.

  • 标签: 透明质酸钠 MRNA 基因表达 金属蛋白酶-1 金属蛋白酶-3 组织抑制
  • 简介:AIM:Todeterminetheexpressionsofinduciblenitricoxidesynthase(iNOS)andmatrixmetalloproteinase-9(MMP-9)inhepatocellularcarcinoma(HCC)andtoinvestigatetherelationshipbetweeniNOSandMMP-9expressionandtheireffectsonangiogenesisandprogressionofHCC.METHODS:Tnthisstudy,weexaminediNOS,MMP-9,andCD34expressioninspecimenssurgicallyremovedfrom32HCCpatientsand7normallivertissuesbyimmunohistochemicalstaining.Meanwhile,microvesseldensity(MVD)wasdeterminedasamarkerofangiogenesisbycountingCD34-positivecells.RESULTS:ThepositiveratesofiNOSandMMP-9expressionwere71.88%(23/32)and78.13%(25/32)inHCC.MMP-gexpressionwassignificantlycorrelatedwithtumorsize,capsulestatus,TNMstage,andriskofHCCrecurrence(P=0.032,P=0.033,P=0.007,andP=0.001,respectively).TherewasalsoasignificantrelationshipbetweeniNOSexpressionandcapsulestatusandriskofHCCrecurrence(P=0.04gandP=0.004,respectively),butnocorrelationbetweeniNOSexpressionandtumorsizeandTNMstage.TherewasapositiveassociationbetweenMVDandTNMstageandriskofHCCrecurrence(P=0.037andP=0.000,respectively).ThecountofMVDwassignificantlydifferentindifferentiNOSandMMP-9immunoreactivitygroups(F=17.713and17.097,P=0.000andP=0.000,respectively).TheexaminationofSpearman'srankcorrelationcoefficientshowedthattherewasasignificantpositivecorrelationbetweenMVDandiNOS,MMP-9immunoreactivity(r=0.754and0.751,P=0.000andP=0.000,respectively).TherewasalsoasignificantassociationbetweenMMP-9andiNOSexpressioninHCC(P=0.010).CONCLUSION:Nitricoxide(NO)producedbyiNOScouldmodulateMMP-9productionandthereforecontributetotumorcellangiogenesisandinvasionandmetastasisinHCC.ThestrongexpressionofiNOSandMMP-9inHCCmaybehelpfulinevaluatingtherecurrenceofHCC,predictingpoorprognosis.ForpatientswithstrongexpressionofMMP-9andiNOS,theoptimaltreatmentschemen

  • 标签: 一氧化氮 金属蛋白酶-9 基因表达 肝细胞癌
  • 简介:Objective:Toinvestigatetheexpressionofmatrixmetalloproteinase-7(MMP-7)andFasligand(FasL)ingastriccancerandexploretheirroleinprogressionofgastriccancer.Methods:Formalin-fixedparaffinandembeddedtissuesofprimarygastriccancerandadjacentnon-tumormucosafrom113caseswereevaluatedforMMP-7,FasLandCapase-3expressionbystreptavidin-peroxidase(S-P)immunohistochemistry.Theexpressionofthefirsttwoproteinsincancercellsofprimaryfociwascomparedwithclinicopathologicalparametersoftumors.WealsoobservedthecorrelationofMMP-7andFasLexpressionwithCaspase-3expressionincancercellsofprimaryfoci.Results:MMP-7positiveimmunostainingwaslessfrequentlydetectedinadjacentepithelialcellsthanincancercellsofprimaryfociofgastriccancer(P<0.05,29.2%vs69.0%),andsowasFasL(P<0.05,34.5%vs54.0%).MMP-7expressionwasassociatedwithtumorsize,Borrmann'sclassification,invasivedepth,metastasisandTNMstaging(P<0.05),butnotwithgrowthpattern,Lauren'sclassification,orhistologicalclassification(P>0.05).FasLexpressionwascorrelatedwithtumorsize,invasivedepth,metastasis,Lauren'sclassification,histologicalclassification(P<0.05),whilenotwithBorrmann'sclassification,TNMstagingorgrowthpattern(P>0.05).CancercellsofprimaryfociexpressedlessCaspase-3thantheiradjacentepithelialcells(P<0.05,32.7%vs50.4%).TherewasanobviouscorrelationbetweenFasL,MMP-7andCaspase-3expressionincancercellsofprimaryfoci(P<0.05).Co-expressionofMMP-7andFasLparalleledwithCaspase-3expressionincancercellsofprimaryfoci(P<0.05).Conclusion:MMP-7andFasLexpressionwasup-regulatedingastriccarcinogenesisandwasprincipallyinvolvedinprogressionofgastriccancer.FasLexpressioncouldreflectthedifferentiationofgastriccancercellsandunderliethemolecularmechanismsofdifferentpathwaysofgastrictumorigenesis.Co-expressionofMMP-7andFasLcouldhaveapoptosis-inducingeffe

  • 标签: FASL MMP-7 基质金属蛋白酶-7 胃癌 基因表达
  • 简介:BACKGROUND:Matrixmetalloproteinase-9(MMP-9)expressionincreaseswithintracerebralhemorrhage,andparticipatesinthepathophysiologicalprocessesofsecondarybraininjuryafterintracerebralhemorrhage.OBJECTIVE:ToinvestigatetheeffectsofmildhypothermiaonMMP-9expressionandbrainedemaintheperihematomalregionofexperimentalintracerebralhemorrhagerats.DESIGN,TIMEANDSETTING:Therandomized,controlledexperimentwasperformedattheCentralLaboratoryofShandongProvincialHospitalbetweenMayandSeptember2007.MATERIALS:Seventy-two,Wistar,malerats,12-weeksold,wereusedforthisstudy.Rabbitanti-MMP-9primaryantibodywaspurchasedfromBoster,China.METHODS:Wistarratswereequallyandrandomlydividedintonormothermiaandmildhypothermiagroups.Thetwogroupseachcomprisedcontrol,6-hourintracerebralhemorrhage,24-hourintracerebralhemorrhage,48-hourintracerebralhemorrhage,72-hourintracerebralhemorrhage,and1-weekintracerebralhemorrhagesubgroups,withsixratsineachsubgroup.Ratmodelsofintracerebralhemorrhagewereestablishedbyinjecting100μLofautologousbloodintotheratcaudatenucleus.Ratsinthemildhypothermiagroupreceivedfourhoursoflocalmildhypothermiaimmediatelyfollowingtheinjection.Intracerebraltemperaturewasmaintainedat(33±0.5)℃.Subsequently,intracerebraltemperaturewasspontaneouslyrecoveredat25℃.Ratsinthecontrolsubgroupwerenotinjectedwithautologousbloodandreceivedonlywithintracerebralhemorrhage.MAINOUTCOMEMEASURES:BrainwatercontentandMMP-9expressionsurroundingthehematomaregion.RESULTS:MMP-9expressionincreasedat6hours,andbrainedemareachedapeakat48hoursafterintracerebralhemorrhage.MMP-9expressionwassignificantlydecreasedinthemildhypothermiagroupcomparedwiththenormothermiagroupateachtimepoint(P<0.05).CONCLUSION:MildhypothermiacansignificantlyinhibitMMP-9overexpressionandrelievebrainedemafollowingintracerebralhemo

  • 标签: 大脑内出血 降低体温作用 MMP-9表达 脑损伤
  • 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:

  • 标签: 大脑 再灌注损伤 血液 分析方法
  • 简介:AbstractBackground:Histone deacetylase 4 (HDAC4) regulates chondrocyte hypertrophy and bone formation. The aim of the present study was to explore the effects of HDAC4 on Interleukin 1 beta (IL-1β)-induced chondrocyte extracellular matrix degradation and whether it is regulated through the WNT family member 3A (WNT3A)/β-catenin signaling pathway.Methods:Primary chondrocytes (CC) and human chondrosarcoma cells (SW1353 cells) were treated with IL-1β and the level of HDAC4 was assayed using Western blotting. Then, HDAC4 expression in the SW1353 cells was silenced using small interfering RNA to detect the effect of HDAC4 knockdown on the levels of matrix metalloproteinase 3 (MMP3) and MMP13 induced by IL-1β. After transfection with HDAC4 plasmids, the overexpression efficiency was examined using Real-time quantitative polymerase chain reaction (qRT-PCR) and the levels of MMP3 and MMP13 were assayed using Western blotting. After incubation with IL-1β, the translocation of β-catenin into the nucleus was observed using immunofluorescence staining in SW1353 cells to investigate the activation of the WNT3A/β-catenin signaling pathway. Finally, treatment with WNT3A and transfection with glycogen synthase kinase 3 beta (GSK3β) plasmids were assessed for their effects on HDAC4 levels using Western blotting.Results:IL-1β downregulated HDAC4 levels in chondrocytes and SW1353 cells. Furthermore, HDAC4 knockdown increased the levels of MMP3 and MMP13, which contributed to the degradation of the extracellular matrix. Overexpression of HDAC4 inhibited IL-1β-induced increases in MMP3 and MMP13. IL-1β upregulated the levels of WNT3A, and WNT3A reduced HDAC4 levels in SW1353 cells. GSK-3β rescued IL-1β-induced downregulation of HDAC4 in SW1353 cells.Conclusion:HDAC4 exerted an inhibitory effect on IL-1β-induced extracellular matrix degradation and was regulated partially by the WNT3A/β-catenin signaling pathway.

  • 标签: Histone deacetylase 4 Matrix metalloproteinase 13 Matrix metalloproteinase 3 Osteoarthritis WNT3A
  • 简介:Basementmembranedegradationandblood-brainbarrierdamageappearaftercerebralinfarction,severelyimpactingneuronalandbrainfunctioning;however,theunderlyingpathogeneticmechanismsremainpoorlyunderstood.Inthisstudy,weinducedcerebralinfarctioninstrokepronespontaneouslyhypertensiveratsbyintragastricadministrationofhigh-sodiumwater(1.3%NaCl)for7consecutiveweeks.Immunohistochemicalandimmunofluorescenceassaysdemonstratedthat,comparedwiththenon-infarctedcontralateralhemisphere,stroke-pronespontaneouslyhypertensiveratsonnormalsodiumintakeandWistar-Kyotorats,matrixmetalloproteinase-9expression,thenumberofbloodvesselswithdiscontinuouscollagenIVexpressionandmicrovesseldensityweresignificantlyhigher,andthenumberofcontinuouscollagenIV-positivebloodvesselswaslowerintheinfarctborderzonesofstroke-pronespontaneouslyhypertensiveratsgivenhigh-sodiumwater.Linearcorrelationanalysisshowedmatrixmetalloproteinase-9expressionwaspositivelycorrelatedwiththenumberofdiscontinuouslycollagenIV-labeledbloodvesselsandmicrovesseldensityincerebralinfarctsofstroke-pronespontaneouslyhypertensiverats.Theseresultssuggestthatmatrixmetalloproteinase-9upregulationisassociatedwithincreasedregionalangiogenesisanddegradationofcollagenIV,themajorcomponentofthebasallamina,instroke-pronespontaneouslyhypertensiveratswithhigh-sodiumwater-inducedfocalcerebralinfarction.

  • 标签: 基质金属蛋白酶-9 自发性高血压大鼠 血管生成 脑梗塞 基底膜 中风
  • 简介:Alongwithnecessariesappliedandthegoingdeeplyintotheresearch,thattheuni-tarymatrixandHermitematrixarepopularizedinmanykinds,andinthispaperuni-versalunitarymatrixanduniversal(oblique)Hermitematrixarestudiedfurther,andthismustbeusefulformatrixtheoryandapplications(likeoptimizationtheory,symplecticgeometryandphysicsetc).Inthepaper,Cm×nshowsm×ncompoundmatrixset,Cnm×nshowsnstepcompoundinvertiblematrixset,A*showsconjugatetransposematrixofA,

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  • 简介:Inthispaper,westudyseveraliterativemethodsforfindingthemaximal-likesolutionofthematrixequationX+A~*X~(-2)A=I,anddeducesomepropertiesofthemaximal-likesolutionwiththesemethods.

  • 标签: 矩阵方程 迭代法 恒等式 复矩阵
  • 简介:在这份报纸,积极明确的矩阵functionals在一套方形的integrable矩阵上定义珍视的功能被介绍并且学习。最好的近似问题以矩阵Fourier系列被解决。Riemann-Lebesgue矩阵性质和Bessel-Parseval矩阵不平等被给。

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  • 简介:Inthispapertheconceptofpositivedefinitebilinearmatrixmomentfunctional.actingonthespaceofallthematrixvaluedcontinuousfunctionsdefinedonaboundedinterval[a,b],isintroduced.ThebestapproximationmatrixproblemwithrespecttosuchafunctionalissolvedintermsofmatrixFourierseries.BasicpropertiesofmatrixFourierseriessuchastheKiemann-Lebesguematrixpropertyandthebessel-parsevalmatrixinequalityareproved.Theconceptoftotalsetvjithrespecttoapositivedefinitematrixfunctionalisintroduced,andthetotallityofanorthonormalsequenceofmatrixpolynomialswithrespecttothefunctional,isestablished.

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  • 简介:InthispaperweintroducetheclassofHermite’smatrixpolynomialswhichappearasfiniteseriessolutionsofsecondordermatrixdifferentialequationsY"-xAY’+BY=0.AnexplicitexpressionfortheHermitematrixpolynomials,theorthogonalitypropertyandaRodrigues’formulaaregiven.

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