简介：Objective:toobserveeffectofendothelin-1(ET-1)onhepaticdamageinducedbyendotoxin.Methods:atotalof90ratswererandomlydividedintocontrolgroup(groupc),endotoxintreatedgroup(groupLPS)andendotoxinplusET-1antibodytreatedgroup(groupLEA).AnobservationwasdoneonthechangesofET-1concentration,andtranscriptionandexpressionofET-1mRNA.Plasmaglutamicpyruvictransaminaseenzyme(GPT),hepaticlactatedehydrogenase(LDH),adenosinetriphosphate(ATP)andmalondialdehyde(MDA)werealsoobservedat3,6,9,12,24hoursaftersaline,endotoxin(10mg·kg^-1)andET-1antibody(dalubine1:2000,2ml·kg^-1)administration.Results:TheresultsindicatedthattheconcentrationofplasmaandhepaticET-1andexpressionofET-1mRNAinliversignificantlyincreasedfollowingendotoxemia.ThehepaticET-1levelswereinverselycorrelatedwiththeATPconcentration,andpositivelyrelatedtotheMDAconcentration.ET-1antibodycouldpartiallyprotecttheliveragainstdamageinducedbyendotoxin.Conclusions:Theseresultssuggestthatendotoxinmay,ontranscriptionandtranslationlevel,leadtoanincreaseofET-1insynthesis.ET-1maycontributetohepaticdamageduringendotoxemia.

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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.

简介：Objective:Toobservetheocularhistopathologicalchangesaftereyeballenucleationinducedbycornealtrauma.Methods:Lightmicroscopicexaminationwasdoneon117eyeballspecimensenucleatedaftercornealtrauma(18withcornealfissureand99withcornealperforatingtrauma).Results:Acute,subacuteorchronicinflammatorychanges,andfibrousmembraneformationwereobservedinwell-closedcornealwounds,whereasinflammation,atrophyandscarwereobservedinthefocaltissues.Butatthelateperiod,secondaryglaucoma,retinaldetachment,endophthalmitisandeyeballatrophyresultedinblindness.Cornealfistulawasobservedinthosewithinadequatecureofwoundscausedbyingrowthofcornealepithelium,embedmentofirisandvitreousbody,andlargeareaofcentrallylocatedtissuedeficiencyofthecorneal.Ahighincidenceofendophthalmitiswasnotedduetothepresenceofcornealfistula.Severeinflammationwasobservedintheanteriorsegmentaltissueswithfibrousinfiltrationintheanteriorchamber,whichmightresultinrapiddestructionoftheeyeballs.Conclusions:Ocularpathologyvarieswiththedifferenceoftheposition,form,sizeandclosingconditionsofthecorneallacerationaftertrauma.

简介：Objective:Tomonitorthesystemicgeneexpressionprofileinamurinemodeloflipopolysaccharide-inducedacutelunginjury.Methods:Acutelunginjurywasinducedbyintratrachealinjectionoflipopolysaccharidein3mice.Another3normalmicereceivingsamevolumeofnormalsalineweretakenasthecontrols.Thecomprehensivegeneexpressionprofilewasmonitoredbytherecentlymodifiedlongserialanalysisofgeneexpression.Results:Atotalof24670tagsrepresenting12168transcriptsinthecontrolmiceand26378tagsrepresenting13397transcriptsinthemicewithlunginjurywereidentifiedrespectively.Therewere11transcriptsincreasingand7transcriptsdecreasingmorethan10foldsinthelipopolysaccharide-treatedmice.ThemostoverexpressedgenesinthemicewithlunginjuryincludedserumamyloidA3,metallothionein2,lipocalin2,cyclin-dependentkinaseinhibitor1A,lactatedehydrogenase1,melatoninreceptor,S100calcium-bindingproteinA9,natriureticpeptideprecursor,etc.Mitogenactivatedproteinkinase3,serumalbumin,complementcomponent1inhibitor,andATPsynthasewereunderexpressedinthelunginjurymice.Conclusions:Serialanalysisofgeneexpressionprovidesamolecularcharacteristicofacutelunginjury.

简介：Aim:ToobservetheapoptoticchangesfollowingexposuretoEMPandtoexplorethepossibleinjurymechanisminNIH-3T3fibroblasts.Methods:FollowingNIH-3T3cellswereexposedtoEMP,theproliferationandviabilityofNIH-3T3fibroblastswereestimatedbyhemacytometerandMTTMeasurements.Apoptoticratewasmeasuredbyflowcytometer.TheimnmohistochemicalSPmethodwasusedtodeterminebcl-2,p53.ThepositivelystainedcellswereanalyzedwithCMIAS-Ⅱimageanalysissystematamagnification400.AlldatawereanalyzedbySPSS8.0software.Results:TheproliferationandviabilityofNIH-3T3cellsweremarkedlyinhibitedandsignificantapoptosiswasinducedfollowingexposuretoEMP.EMPcouldincreasethenumberofnon-adherentcells,thehighestratio(33.9%)ofnon-adherentcellsalsooccurredat6h.TheAs70valueofMTTdecreasedimmediatelyat1h,6hfollowingthecellswereexposedascomparedwiththecontrol(P＜0.05).Thehighestratioofapoptosiswas15.07%at6h,thendecreasedgradually.Down-regulationofbcl-2andup-regulationofp53wereinducedbyEMP(P＜0.05).Conclusions:EMPcouldpromoteapoptosisofNIH-3T3fibroblasts.EMPcouldalsodown-regulatebcl-2levelandup-regulatep53levelinNIH-3T3fibroblasts.Bcl-2andp53genemaytakepartintheprocessofapoptosis.

简介：ＴＢｕｒｎＲｅｓｅａｒｃｈＩｎｓｔｉｔｕｔｅ，ＳｏｕｔｈｗｅｓｔｅｒｎＨｏｓｐｉｔａｌ，ＴｈｉｒｄＭｉｌｉｔａｒｙＭｅｄｉｃａｌＣｏｌｅｇｅ，Ｃｈｏｎｇｑｉｎｇ４０００３８，Ｃｈｉｎａ（ＣｈｉＬＸ，ＹａｎｇＺＣ，ＷａｎｇＸａｎｄＬｉＡ）Ｔｈｉｓｓｔ...

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简介：Objective:Impairedactivefluidtransportofalveolarepitheliummayinvolveinthepathogenesisandresolutionofalveolaredema.Thcobjectiveofthisstudywastoexplorethechangesinalveolarepithelialliquidclearanceduringlungedemafollowingacutelunginjuryinducedbyoleicacid.Methods:Forty-eightWistarratswererandomlydividedintosixgroups,I.e.,injured,amiloride,ouabain,amilorideplusouabainandterbutalinegroups.Twenty-fourhoursaftertheinductionofacutelunginjurybyintravenousoleicacid(0.25ml/kg),5％albuminsolutionwith1.5μCi125Ⅰ-labeledalbumin(5ml/kg)wasdeliveredintobothlungsviatrachea.Alveolarliquidclearance(ALC),extravascularlungwater(EVLW)contentandarterialbloodgasesweremeasuredonehourthereafter.Results:At24haftertheinfusionofoleicacid,theratsdevelopedpulmonaryedemaandseverehypoxemia,withEVLWincreasedby47.9％andALCdecreasedby49.2％.Additionofeither2×10-3Mamilorideor5×10-4MouabaintotheinstillationfurtherreducedALCandincreasedEVLW.ALCincreasedbyapproximately63.7％andEVLWdecreasedby46.9％withimprovedhypoxemiaintheTerbutaline(10-4M)group,comparedthoseininjuredrats.AsignificantnegativecorrelationwasfoundbetweentheincrementofEVLWandthereductionofALC.Onclusions:Activefluidtransportofalveolarepitheliummightplayaroleinthepathogenesisoflungedemainacutelunginjury.

简介：Objective:Todeterminetheroleofhemoglobin(HB)-inducedhemeoxygenase-1(HO-1)ininjuredlungscausedbylimbischemia-reperfusion(I/R)inrats.Methods:Aratmodelofischemiainthehindlimbswasmadebyclampingtheinfrarenalaortawithamicrovascularclip,andlunginjuryoccurredafterreperfusion.ToinducetheexpressionofHO-1inthelungs,Hbwasadministratedintraperitoneallyat16hoursbeforereperfusion.NorthernblottingandWesternblottingwereusedtodetecttheexpressionofHO-1inthelungs,andthecarboxyhemoglobin(COHb)levelinarterialbloodwasassayed.Theeffectofhemoglobin(Hb)ontheinjuredlungsafterlimbI/Rwasdeterminedbymeasuringthechangesoflunghistology,polymorphonuclear(PMN)count,malondialdehyde(MDA)contentandwet-to-dryweightratio(W/D).Zincprotoporphyrin(ZnPP),aninhibitorofHO,wasusedtodeterminewhetherHO-1wasinducedbyHbafterlunginjury.Results:HbledtoasignificantincreaseinHO-1mRNAandproteinexpressioninthelungs,accompaniedbytheincreaseofCOHblevelinarterialblood.Comparedwiththeshamcontrols,thelungPMNcount,MDAcontentandW/Dsignificantlyincreasedat4hoursafterlimbI/R,whichreversedbythepretreatmentwithHbat16hoursbeforereperfusion.ZnPPblockedthisprotectiveroleofHbintheinjuredlungs.Conclusions:HbcaninducethelungHO-1expression,whichplaysanimportantroleinthedefenseagainstI/R-inducedlunginjuryinrats.

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.

简介：Objective:ToinvestigatetheeffectofRadixPaeoniaeRubra(RPR)ontheexpressionofhemeoxygenase(HO-1)andinducednitricoxidesynthase(iNOS)inendotoxin-inducedacutelunginjuryinratsanditsprotectivemechanism.Methods:FortyWistarratsweredividedrandomlyinto5groupswith8ratsineachgroup:salinecontrolgroup(NSgroup),lipopolysaccharidegroup(LPSgroup),RPR-treatmentgroup,RPR-preventiongroupandHemingroup.TheeffectofRPRonproteincontent,theratioofneutrophilesinbronchoalveolarlavagefluid,malondialdehyde(MDA)contentinthelungandtheactivityofserumNOwereobserved.Arterialbloodwasdrawnforblood-gasanalysis.TheexpressionofHO-1andiNOSinlungtissueswasdetectedbyimmunohistochemitryandmorphometrycomputerimageanalysis.Thehistologicalchangesofthelungwereobservedunderlightmicroscope.Results:ComparedwiththatinNSgroup,theexpressionofHO-1andiNOSwasmarkedlyincreasedinLPSgroup(P<0.01).InRPR-treatment,RPR-prevention,andHemingroups,theexpressionofiNOSwassignificantlylower,whiletheexpressionofHO-1washigherthanthatinLPSgroup(P<0.05).Theproteincontent,theratioofneutrophilesinbronchoalveolarlavagefluid,thecontentofMDAandtheactivityofserumNOinLPSgroupweresignificantlyhigherthanthoseinNSgroup(P<0.01).TherewasasignificantdecreaseinthelevelofarterialbicarbonateandpartialpressureofoxygenintheLPSgroup(P<0.01);theseparametersoflunginjuryhowever,weresignificantlylowerinRPR-treatment.RPR-prevention,andHemingroupsthanLPSgroup(P<0.05orP<0.01).ThepathologicchangesoflungtissuesweresubstantiallyattenuatedinRPR-treatment,RPR-prevention,andHemingroupsthanLPSgroup.Conclusions:ThehighexpressionofHO-1reflectsanimportantprotectivefunctionofthebodyduringlipopolysaccharide-inducedacutelunginjury.TheprotectiveeffectofRPRonlipopolysaccharide-inducedacutelunginjuryisrelatedtotheinhibi