简介：Theeffectsofanexogenousnitricoxidedonor(sodiumnitroprusside,SNP),aNOscavenger2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxode(PTIO)andcarboxy-PTIOpotassiumsalt(cPTIO)ontheembryogerminationofSorbuspohuashanensiswerestudiedinapetridishtest.SNPat0.5–5mmolL-1increasedgerminationpercentage,meantimetogermination,germinationindexandgerminationenergycomparedwiththecontroltodifferentdegrees.Treatmentwith2mmolL-1SNPimprovedgerminationmostsignificantly;embryogerminationpercentageformothertree1(91.11%)andmothertree2(64.44%)weremuchhigherthanthecontrol.Inaddition,excessiveSNPlevelsdidnotenhanceembryogermination.CombinedtreatmentwithSNPandanNOscavengerdelayedembryogermination.TreatmentwithcPTIOinhibitedembryogermination;germinationpercentagewas42.22%andwaslowerthanthatofthecontrol.TheseresultsshowthatlowconcentrationsofexogenousNOcanenhancetheembryogerminationofS.pohuashanensis,providingasimple,effectivewayforpromotinggerminationofS.pohuashanensis.

简介：Nitricoxide(NO)isapleiotropicregulator,criticaltonumerousbiologicalprocesses,includingva-sodilatation,neurotransmissionandmacrophage-mediatedimmunity.Thefamilyofnitricoxidesynthases(NOS)comprisesinducibleNOS(iNOS),endothelialNOS(eNOS),andneuronalNOS(nNOS).Interest-ingly,variousstudieshaveshownthatallthreeisoformscanbeinvolvedinpromotingorinhibitingtheetiologyofcancer.NOSactivityhasbeendetectedintumourcellsofvarioushistogeneticoriginsandhasbeenassociatedwithtumourgrade,proliferationrateandexpressionofimportantsignalingcomponentsassociatedwithcancerdevelopmentsuchastheoestrogenreceptor.ItappearsthathighlevelsofNOSexpression(forexample,generatedbyactivatedmacrophages)maybecytostaticorcytotoxicfortumorcells,whereaslowlevelactivitycanhavetheoppositeeffectandpromotetumourgrowth.Paradoxicallytherefore,NO(andrelatedreactivenitrogenspecies)mayhavebothgenotoxicandangiogenicproperties.IncreasedNO-generationinacellmayselectmutantp53cellsandcontributetotumourangiogenesisbyupregulatingVEGF.Inaddition,NOmaymodulatetumourDNArepairmechanismsbyupregulatingp53,poly(ADP-ribose)polymerase(PARP)andtheDNA-dependentproteinkinase(DNA-PK).Anunderstand-ingatthemolecularleveloftheroleofNOincancerwillhaveprofoundtherapeuticimplicationsforthediagnosisandtreatmentofdisease.

简介：Themanagementofneurologicaldisordershavehugeandincreasinghumanandeconomiccosts.Despitethis,thereisascarcityofeffectivetherapeutics,andthereisanextremeurgencyfornewandrealtreatments.Inthisshortreviewweanalyzesomepromisingadvancementsinthesearchofnewbioactivemoleculestargetingneuronalnitricoxidesynthase(nNOS),anenzymedeputedtothebiosynthesisofnitricoxide(NO).Indifferentconditionsofneuronaldamages,thismoleculeisoverproduced,contributingtothepathogenesisandprogressionofneuronaldiseases.TwomainapproachestomodulatenNOSarediscussed:afirstoneconsistinginthedirectinhibitionoftheenzymebymeansofsmallorganicmolecules,whichcanbealsoactiveagainstotherdifferenttargetsinvolvedinsuchdiseases.AsecondsectionisdedicatedtomoleculesabletopreventtheformationoftheternarycomplexN-methyl-D-aspartate(NMDA)-typeglutamatereceptors,postsynapticdensity-95(PSD95)protein-nNOS,whichisnecessarytoactivatethelatterforthebiosynthesisofNO.

简介：AIM:Toassessthemechanismsofprotectiveactionbydifferentmildirritantsthroughmaintenanceofgastricmucosalintegrityandmodulationofmucosalnitricoxide(NO)inexperimentalgastritisrats.METHODS:Etcher200mL/Lethanol,50g/LNaGor0.3mol/LHClwaspretreatedtonormalor800mL/Lethanol-inducedacutegastritisSprague-Dawleyratsbeforeasubsequentchallengewith500mL/Lethanol.Bothmacroscopiclesionareasandhistologicaldamagescoresweredeterminedinthegastricmucosaofeachgroupofanimals.Besides,gastricmucosalactivitiesofNOsynthaseisoformsandofsuperoxidedismutase,alongwithmucosallevelofleukotriene(LT)C4weremeasured.RESULTS:Macroscopicmucosaldamageswereprotectedby200mL/Lethanoland50g/LNaCIingastritisrats.However,although200mL/Lethanolcouldprotectthesurfacelayersofmucosalcellsinnormalanimals(protectionattenuatedbyNG-nitro-L-argininemethylester),nocytoprotectionagainstdeeperhistologicaldamageswasfoundingastritisrats.Besides,inducibleNOsynthaseactivitywasincreasedinthemucosaofgastritisanimalsandunalteredbymildirritants.Nevertheless,theelevationinmucosalLTC4levelfollowing500mL/Lethanoladministrationandundergastritisconditionwassignificantlyreducedbypretreatmentofallthreemildirritantsinbothnormalandgastritisanimals.CONCLUSION:Thesefindingssuggestthattheaggravated500mL/Lethanol-evokedmucosaldamagesundergastritisconditioncouldbeduetoincreasedinducibleNOandLTC4productioninthegastricmucosa.Only200mL/Lethanolistruly'cytoprotective'atthesurfaceglandularlevelofnongastritismucosa.Furthermore,themacroscopicprotectionofthethreemildirritantsinvolvesreductionofLTC4levelinbothnormalandgastritismucosa,implicatingpreservationofthevasculature.

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简介：BACKGROUND:Oxidativestressplaysanimportantroleinthepathophysiologyofepilepsy.Glutathione,knownasoneofthecompoundsofantioxidantdefense,hasbeenshowntoinhibitconvulsions.Nitricoxidehasaproconvulsanteffectonapentylenetetrazole-inducedanimalmodel.OBJECTIVE:Toevaluatetheeffectsofglutathioneadministrationonnitricoxidelevelsinbrainregionsofconvulsiveandkindlingpentylenetetrazole-inducedseizuremodels.DESIGN,TIME,ANDSETTING:Arandomized,controlled,animalexperiment.ThestudywasperformedattheDepartmentofPhysiology,GaziantepUniversityandDepartmentofChemistry-Biochemistry,KahramamarasSutcuImamUniversityin2006.MATERIALS:PentylenetetrazoleandglutathionewerepurchasedfromSigma,USA.METHODS:Atotalof80micewereassignedto8groups(n=10):normalcontrol,salinecontrol(1mLnormalsaline),convulsivepentylenetetrazole(singleintraperitonealadministrationofpentylenetetrazole,60mg/kg),convulsivepentylenetrazoleplusglutathione(singleadministrationof60mg/kgpentylenetetrazoleand200mg/kgglutathione),five-doseglutathione(intraperitonealinjectionof200mg/kgglutathionerespectivelyat1,3,5,7,and10days),single-doseglutathione(singleadministrationof200mg/kgglutathione),pentylenetetrazolekindling(intraperitonealadministrationofpentylenetetrazoleof40mg/kgat1,3,5,7,and10days),andpentylenetetrazolekindlingplusglutathionegroup(intraperitonealinjectionof40mg/kgpentylenetetrazoleand200mg/kgglutathionerespectivelyat1,3,5,7,and10days).MAINOUTCOMEMEASURES:Allmiceweresacrificed1hourafterthelastadministration.Brainnitricoxidelevelsweredeterminedbyspectrophotometry.RESULTS:Therewerenosignificantdifferencesinnitricoxidelevelsbetweenthenormalcontrol,salinecontrol,five-doseglutathione,andsingle-doseglutathionegroups(P>0.05).Nitricoxidelevelsinthecerebralhemisphereandcerebellumweresignificantlylessintheconvulsivepentylenetetrazolegroup,comparedwiththeconvu

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简介：ObjectivesTostudythechangesofnitricoxide,angiotensinⅡandsuperoxideanioninrenalarteryhypertensionpathogenesis.MethodsMaleWistarratsweighing256-285gweredividedinto5groupsrandomly,10ratsofeachgroup.Controlgroup:falseoperationwasmadeandroutinedietwasgiven;Ligaturegroup:leftrenalarterywasligatureduncompletelyandroutinedietwasgiven;Ligature+Losartangroup:leftrenalarterywasligatureduncompletelyandLosartan20mg·kg^-1·d^-1wasaddedinthedrinkingwater;Ligature+L-Arggroup:leftrenalarterywasligatureduncompletelyandL-Arg2g·kg^-1·d^-1wasaddedinthedrinkingwater;Ligature+L-Arg+Losartangroup:leftrenalarterywasligatureduncompletelyandL-Arg2g·kg^-1·d^-1andLosartan20mg·kg^-1·d^-1wasaddedinthedrinkingwater.Bloodpressureandheartrateweremeasuredbeforeandattheendoftheexperiment.Oneweekafterligature,bloodwasdrawntodetermineangiotensinⅡ,cGMP,nitricoxide,nitricoxidesynthase(NOS),O2^-,superoxidedismutase(SOD).ResultsSystolicbloodpressurewashigherinligaturegroupthanthatincontrolgroup(p<0.05),systolicbloodpressurewasmuchlowerinligature+Losartangroupthanthatinligaturegroup.Heartratedidnotchangesignificantlyafterexperiment(p>0.05).AngⅡwashigherinligaturegroupthanthatincontrolgroup,evenmuchhigherinligature+Losartangroup(p<0.01).TherewasnodifferenceofcGMPineachgroup(p>0.05).TheconcentrationofNOwaslowerinligaturegroup(p<0.05),NOwashigherinligature+L-Arg+Losartangroupthanthatinligaturegroup(p<0.05).O2^-washigherinligaturegroupandligature+L-Arggroupthanthatincontrolgroup(p<0.05),O2^-waslowerinligature+Losartangroupthanthatinligaturegroup(p<0.05).ThelevelofSODwaslowerinligaturegroupthanthatincontrolgroup(p<0.05),higherinligature+L-Arggroupandligature+L-Arg+Losartangroupthanthatinligature

简介：Aseriesoffuroxan-basednitricoxide-releasingmatrinederivatives(10a-f)weresynthesized.Thebiologicalevaluationshowedthatcompounds10a,10b,10eand10fhadstrongercytotoxicactivitiesthan5-fluorouracilagainsthumanhepatomacells(HepG2)invitro.

简介：Anovelamperometricsensorforthedeterminationofnitricoxidewasdevelopedbycoatingpolythionine/nafiononaglassycarbonelectrode.Thissensorexhibitedagreatenhancementtotheoxidationofnitricoxide.Theoxidationpeakcurrentswerelineartotheconcentrationofnitricoxideoverthewiderangefrom3.6×10-7to6.8×10-5mol.L-1,andthedetectionlimitwas7.2×10-8mol.L-1.Experimentalresultsshowedthatthisnitricoxidesensorpossessedexcellentselectivityandlongerstability.NOreleasingfromratkidneywasmonitoredbythissensor.

简介：Objective:Toanalyzetheexpressionofinduciblenitricoxidesynthase(iNOS),endothelialnitricoxidesynthase(eNOS)andvascularendothelialgrowthfactor(VEGF)inhepatocellularcarcinoma(HCC)anditsrelationtoangiogenesis.Methods:Tissuesectionsfrom71HCCpatientswereexaminedimmunohistochemicallyforproteinexpressionofiNOS,eNOS,andVEGF.Microvessaldensity(MVD)wascountedbyendothelialcellsimmunostainedbyanti-CD34antibody.Results:PositiveimmunostainingforiNOS,eNOSwasdetectedin83.1%and85.9%ofHCCrespectively.INOSandeNOSwerenotdetectedinnormalhepatictissue.MVDwas34.3±1.5/HPand38.6±1.6/HPinHCCwithpositivestainingforiNOSandVEGFwhileitwas31.2±2.8/HP,and22.4±2.0/HPinHCCwithnegativestainingforiNOSandVEGF(P<0.01).AcorrelationbetweenNOSexpressionandVEGFinHCCwasnotobserved.Conclusion:iNOSandeNOSmayplayaroleinmalignanttransformationfpost-hepaticcirrhosis.TheexpressionofiNOSandVEGFfavorsangiogenesisofHCC.

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简介：良性的prostatic增生(BPH)的精确原因论仍然保持不清楚；然而，它被知道煽动性的过程有的那免疫学的在BPH开始和前进的致病的一个角色。氮的氧化物synthase2(NOS2)可诱导的表示密切与prostatic疾病被相关，包括前列腺癌症和BPH。这研究的目的是调查在NOS2多型性和BPH之间的关系。与205控制和229个BPH题目的一个队，我们genotyped在NOS2基因的三单个核苷酸多型性(SNP)，包括rs2779248(倡导者，?278T/C)，rs10459953(5鈥?untranslated区域)和rs2297518(exon16，错误感觉，Ser608Leu)，用直接定序和限制碎片长度多型性。在控制和BPH题目之间的genotypic和突变而产生之遗传的频率被比较，并且在BPH题目之中的协会被分析。SNPStats，SNPAnalyzer和HelixTree计划被用来分析SNP。在控制和BPH题目之间的SNP上没有协会。当BPH题目被分析时，在低、高的前列腺特定的抗原组之间的SNP上没有协会。然而，一SNP(rs10459953，机会比率[或]=0.44，95%信心间隔[CI]=0.29鈥?.65，P<0.0001，在codominant当模特儿；或=0.23，95%CI=0.12鈥?.46，P<0.0001，在里面主导的模型；并且或=0.46，95%CI=0.24鈥?.86，P=0.015，在后退的模型)在BPH与prostatic体积被联系。我们在BPH与小、大的prostatic体积在在题目之间的NOS2SNP(rs10459953)的遗传型频率检测了一个强壮的协会。结果建议NOS2可以在BPH与prostatic体积被联系。

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

简介：Cadmium(Cd)ishighlytoxictoplants,animals,andhumans.Limitedinformationisavailableontheroleofnitricoxide(NO)and/or24-epibrassinolide(EBR)inresponseofplantstoCdstress.Inthisstudy,ahydroponicexperimentwasperformedtoinvestigatetheeffectsofNOand/orEBRonpeanutplantssubjectedtoCdstress(200μmolL-1)withsodiumnitroprusside(SNP,anexogenousNOdonor)(250μmolL-1)and/orEBR(0.1μmolL-1)addition.TheresultsshowedthatCdexposureinhibitedplantgrowth,andthisstresswasalleviatedbyexogenousNOorEBR,andespeciallythecombinationofthetwo.TreatmentwithCdinhibitedthegrowthofpeanutseedlings,decreasedchlorophyllcontent,andsignificantlyincreasedtheCdconcentrationinplants.Furthermore,theconcentrationofreactiveoxygenspecies(ROS)markedlyincreasedinpeanutseedlingsunderCdstress,resultingintheaccumulationofmalondialdehyde(MDA)andprolineinleavesandroots.UnderCdstress,applicationsofSNP,EBR,andespeciallythetwoincombinationsignificantlyreducedthetranslocationofCdfromrootstoleaves,increasedthechlorophyllcontent,decreasedtheconcentrationsofROS,MDA,andproline,andsignificantlyenhancedtheactivitiesofsuperoxidedismutase(SOD),peroxidase(POD),andcatalase(CAT)inpeanutseedlings.ExogenousNOand/orEBRalsostimulatedtheactivitiesofnitratereductase(NR)andnitricoxidesynthase(NOS)andincreasedthecontentsofantioxidants,suchasascorbicacid(AsA)andreducedglutathione(GSH).Furthermore,exogenousNOand/orEBRenhancedCdaccumulationinthecellwallandthusdecreasedCddistributionintheorganellesintheroots.Theconcentrationsofcalcium(Ca),iron(Fe),magnesium(Mg),andzinc(Zn)werealsoregulatedbyexogenousNOorEBR,andespeciallybythetwoincombination.TheseresultsindicatedthatSNPandEBR,aloneandparticularlyincombination,canmitigatethenegativeeffectsofCdstressinpeanutplants.

简介：Nitricoxidehasplayedanimportantroleinmanyphysiologicalandpathologicalprocessesasakindofimportantgassignalmolecules.Inthiswork,anewfluorescentprobeLysoNO-NaphfordetectingNOinlysosomesbasedon1,8-naphthalimidewasreported.LysoNO-Naphhassub-groupsofo-phenylenediamineasaNOreactionsiteand4-(2-aminoethyl)-morpholineasalysosome-targetablegroup.Thisprobeexhibitedgoodselectivityandhighsensitivity(4.57mmol/L)towardNOinawidepHrangefrom4to12.Furthermore,LysoNO-NaphcanbeusedforimagingNOinlysosomesinlivingcells.

简介：瞄准：为了在ischemia-reperfusion(红外)上调查rosuvastatin的保护的效果，并且在内皮的氮的氧化物synthase(eNOS)的表示上决定这个代理人的效果，在老鼠导致了小肠的损害和发炎蛋白质。方法：肠的损坏被为30min夹钳优异mes伤寒动脉和腹的箱子在男Sprague-Dawley老鼠导致，为60min由灌注列在后面。在生理盐水溶解的Rosuvastatinintraperitoneally被管理在局部缺血前的60min。肠的粘膜损害和发炎的严厉被几个生物化学的标记，以及由组织检查所见评估。eNOS的蛋白质层次被西方的污点决定。结果：当粘膜的索引损坏，管腔内血红素和蛋白质的层次显著地在假冒操作组与那些相比在红外组被增加。然而，这些增加被处理显著地以一种剂量依赖者方式与rosuvastatin禁止。rosuvastatin的保护的效果被组织检查所见也证实。到红外的小肠的暴露导致了thiobarbituric的重要增加描绘的粘膜发炎酸反应的物质，联系织物的myeloperoxidase活动，和老鼠的粘膜内容导致cytokine的嗜中性的chemoattractant-1(CINC-1)和肿瘤坏死factor-alpha(TNF-alpha)。在红外以后的煽动性的参数的这些增加被预告的处理显著地在10mg/kg的剂量与rosuvastatin禁止。而且，CINC-1和TNF-alpha的mRNA表示在红外以后被增加，并且这增加被rosuvastatin也禁止。eNOS的粘膜蛋白质层次在红外期间减少了，但是在与rosuvastatin对待的老鼠被保存。结论：Rosuvastatin禁止老鼠红外导致的肠的损害和发炎，和它的保护与eNOS的保藏被联系蛋白质。

简介：Objective:Tostudytheeffectofnitricoxide-inducedtyrosinephosphorylationoflarge-conductancecalcium-activatedpotassium(BKCa)channelαsubunitonvascularhyporesponsivenessinrats.Methods:Atotalof46Wistarratsofeithersex,weighing250g±20g,wereusedinthisstudy.Modelsofvascularhyporesponsivenessinducedbyhemorrhagicshock(30mmHgfor2hours)invivoandbyL-arginineinvitrowereestablishedrespectively.Thevascularresponsivenessofisolatedsuperiormesentericarteriestonorepinephrinewasobserved.TyrosinephosphorylationofBKCaαsubunitwasevaluatedwithmethodsofimmunoprecipitationandWesternblotting.Results:Inthesmoothmusclecellsofthesuperiormesentericarteries,theexpressionofBKCaαsubunittyrosinephosphorylationincreasedfollowinghemorrhagicshock,andL-argininecouldinduceBKCachannelαsubunittyrosinephosphorylationinatime-anddose-dependentmanner.L-NAME(Nω-nitro-L-arginine-methyl-ester),anitricoxidesynthetaseinhibitor,couldpartlyrestorethedecreasedvasoresponsivenessofthesuperiormesentericarteriesafterhemorrhagicshockinrats.Down-regulatingtheproteintyrosinephosphorylationwithgenistein,awidely-usedspecialproteintyrosinekinaseinhibitor,couldpartlyimprovethedecreasedvasoresponsivenessofthesuperiormesentericarteriesinducedbyL-arginineinvitro,whileup-regulatingtheproteintyrosinephosphorylationwithNa3VO4,aproteintyrosinephosphataseinhibitor,couldfurtherdecreasethenitricoxide-inducedvascularhyporesponsiveness,whichcouldbepartlyamelioratedby0.1mmol/Ltetrabutylammoniumchloride(TEA),aselectiveBKCainhibitoratthisconcentration.Conclusions:NitricoxidecaninducethetyrosinephosphorylationofBKCaαsubunit,whichinfluencesthevascularhyporesponsivenessinhemorrhagicshockratsorinducedbyL-arginineinvitro.

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