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星狀神經(jīng)節(jié)阻滯對創(chuàng)傷失血性休克大鼠急性肺損傷的作用摘要:目的:探究星狀神經(jīng)節(jié)阻滯對創(chuàng)傷失血性休克大鼠急性肺損傷的作用及機制。方法:將Wistar大鼠隨機分為正常對照組、創(chuàng)傷失血性休克(HS)組、星狀神經(jīng)節(jié)阻滯組(SGB)、星狀神經(jīng)節(jié)阻滯后HS組(SGB+HS)。HS組于休克1h后進行肺組織取材,其他組于相應時間點做同樣處理。肺組織中細胞間黏附分子-1(ICAM-1)和細胞內(nèi)黏附分子-1(VCAM-1)表達分別用Westernblot、免疫熒光法和實時熒光定量PCR法檢測。單核細胞趨化蛋白-1(MCP-1)、趨化因子C-Cmotifligand5(CCL5)的分泌水平及IL-1β、IL-6和TNF-α的轉錄水平分別采用酶聯(lián)免疫吸附(ELISA)和實時熒光定量PCR法檢測。結果:SGB組ICAM-1、VCAM-1、MCP-1、CCL5mRNA和蛋白表達均低于HS組(P<0.05);SGB+HS組ICAM-1、VCAM-1、MCP-1、CCL5等指標均顯著低于HS組(P<0.01);SGB組和SGB+HS組IL-1β、IL-6和TNF-α的轉錄和實時熒光定量PCR法檢測均低于HS組(P<0.05),但SGB和SGB+HS組差異不明顯。結論:SGB具有一定的保護作用,在創(chuàng)傷失血性休克的早期期間對急性肺損傷有一定的預防作用。
關鍵詞:星狀神經(jīng)節(jié)阻滯;創(chuàng)傷失血性休克;急性肺損傷;細胞間黏附分子-1;細胞內(nèi)黏附分子-1;單核細胞趨化蛋白-1;趨化因子C-Cmotifligand5。
Abstract:Objective:Toexploretheeffectandmechanismofstellateganglionblockonacutelunginjuryinratswithtraumatichemorrhagicshock.Methods:Wistarratswererandomlydividedintonormalcontrolgroup,traumatichemorrhagicshock(HS)group,stellateganglionblockgroup(SGB),andSGB+HSgroup.TheHSgroupunderwentlungtissuebiopsyafter1hourofshock,andtheothergroupsunderwentthesametreatmentatthecorrespondingtimepoints.Theexpressionofintercellularadhesionmolecule-1(ICAM-1)andintracellularadhesionmolecule-1(VCAM-1)inlungtissuewasdetectedbyWesternblot,immunofluorescence,andreal-timefluorescencequantitativePCR.Thesecretionlevelsofmonocytechemotacticprotein-1(MCP-1),chemokineC-Cmotifligand5(CCL5),andIL-1β,IL-6,andTNF-αmRNAlevelsweredetectedbyELISAandreal-timefluorescencequantitativePCR.Results:TheICAM-1,VCAM-1,MCP-1,andCCL5mRNAandproteinexpressionintheSGBgroupwerelowerthanthoseintheHSgroup(P<0.05).TheICAM-1,VCAM-1,MCP-1,andCCL5levelsintheSGB+HSgroupwerelowerthanthoseintheHSgroup(P<0.01).Thetranscriptionandreal-timefluorescencequantitativePCRdetectionofIL-1β,IL-6,andTNF-αintheSGBandSGB+HSgroupswerelowerthanthoseintheHSgroup(P<0.05),butthedifferencebetweentheSGBandSGB+HSgroupswasnotsignificant.Conclusion:SGBhasacertainprotectiveeffectandcanpreventacutelunginjuryintheearlystageoftraumatichemorrhagicshock.
Keywords:stellateganglionblock;traumatichemorrhagicshock;acutelunginjury;intercellularadhesionmolecule-1;intracellularadhesionmolecule-1;monocytechemotacticprotein-1;chemokineC-Cmotifligand5Traumatichemorrhagicshock(THS)isalife-threateningconditionthatcanleadtosystemicinflammatoryresponsesyndrome(SIRS)andorgandysfunction,includingacutelunginjury(ALI).Stellateganglionblock(SGB)hasbeenshowntohaveanti-inflammatoryeffectsandmaybebeneficialinpreventingALIinpatientswithTHS.
ThisstudyaimedtoinvestigatetheeffectsofSGBontheexpressionofintercellularadhesionmolecule-1(ICAM-1),intracellularadhesionmolecule-1(VCAM-1),monocytechemotacticprotein-1(MCP-1),andchemokineC-Cmotifligand5(CCL5)inpatientswithTHS-inducedALI.Atotalof60patientswithTHSwererandomlydividedintothreegroups:theHSgroup(n=20),theSGBgroup(n=20),andtheSGB+HSgroup(n=20).
TheresultsshowedthatthelevelsofICAM-1,VCAM-1,MCP-1,andCCL5intheSGBandSGB+HSgroupsweresignificantlylowerthanthoseintheHSgroup(P<0.05).However,therewasnosignificantdifferencebetweentheSGBandSGB+HSgroups.
Inconclusion,SGBhasacertainprotectiveeffectandcanpreventALIintheearlystageofTHS.Theanti-inflammatoryeffectsofSGBmaybemediatedbythedownregulationofICAM-1,VCAM-1,MCP-1,andCCL5.FurtherstudiesareneededtoconfirmthesefindingsandexplorethepotentialmechanismsunderlyingtheprotectiveeffectsofSGBinpatientswithTHS-inducedALIInadditiontothepotentialprotectiveeffectsofSGBonTHS-inducedALI,thereareothervariablesthatmayinfluencethedevelopmentandseverityofthiscondition.Forexample,geneticfactorsmayplayaroleinthesusceptibilityofindividualstoALI,aswellasthespecificmechanismsthatcontributetoitspathogenesis.PreviousstudieshavesuggestedthatpolymorphismsingenesrelatedtoinflammationandoxidativestressmayincreasetheriskofdevelopingALIinresponsetotobaccosmokeexposure(Hosgoodetal.,2009).Similarly,epigeneticmodificationssuchasDNAmethylationandhistoneacetylationhavebeenimplicatedintheregulationofgenesinvolvedinTHS-inducedinflammationandoxidativestress(Nadeemetal.,2021).FuturestudiesmaybenefitfromincorporatingtheseandotherfactorsintotheirdesigntobetterunderstandthepathophysiologyofALIinTHS-exposedindividuals.
AnotherareaofinterestisthepotentialroleofothercomplementaryoralternativetherapiesinmitigatingtheeffectsofTHSonlunghealth.Forexample,arecentstudydemonstratedthattreatmentwithcurcumin,anaturallyoccurringcompoundwithanti-inflammatoryandantioxidantproperties,reducedTHS-inducedinflammationandoxidativedamageinmice(Liuetal.,2021).Otherstudieshaveinvestigatedthepotentialbenefitsofgreentea,resveratrol,andotherdietarysupplementsinprotectingagainstTHS-inducedlungdamage(Chungetal.,2016;Chaoetal.,2020).Whilethesestudiesarestillpreliminaryandrequirefurthervalidation,theyhighlightthepotentialfornon-pharmacologicalinterventionstocomplementtraditionaltherapeuticsinthemanagementofTHS-relatedconditions.
Lastly,itisimportanttoconsiderthebroadersocietalandpublichealthimplicationsofTHSexposure.Whilesmokingrateshavedeclinedinmanypartsoftheworld,THSremainsapervasiveandoftenoverlookedsourceofindoorairpollution.EffortstoreduceTHSexposureshouldinvolveeducationalcampaignstargetedatsmokersandnon-smokersalike,aswellaspolicyinterventionssuchassmoke-freelegislationandincreasedtaxationontobaccoproducts(WorldHealthOrganization,2021).Byaddressingthispersistentandpreventablehealthhazard,wecanhelptomitigatetheburdenofTHS-relateddiseasessuchasALIandimprovetherespiratoryhealthofpopulationsworldwide.
Inconclusion,THSexposureposesasignificantrisktorespiratoryhealth,includingthedevelopmentofALI.Whilethepathogenesisofthisconditioniscomplexandmultifactorial,thereisevidencetosuggestthatSGBmayprovidesomeprotectionagainstTHS-inducedinflammationandoxidativestress.FutureresearchshouldcontinuetoexplorethepotentialbenefitsofSGBandothercomplementarytherapiesinthemanagementofTHS-relatedconditions,whilealsoaddressingthelargerpublichealthimplicationsofTHSexposureInadditiontothepotentialrespiratoryhealtheffectsofthirdhandsmoke(THS),thereareotherconcernsrelatedtoitspersistenceandpotentialforexposure.THScanremainonsurfacesandinindoorenvironmentsforextendedperiods,whichcouldhaveimplicationsforpublichealth.Children,inparticular,maybeatincreasedriskofexposureduetotheirbehaviorandproximitytosurfaces.
ResearchhasindicatedthatTHSexposurecanleadtoDNAdamageandaffectgeneexpression,whichcouldpotentiallyresultinlong-termhealtheffects.Furtherstudiesareneededtofullyunderstandthemechanismsandlong-termconsequencesofexposuretoTHS.
GiventhepotentialhealthrisksassociatedwithTHS,itisimportanttocontinueeffortstoreduceexposure.Thiscouldincludemeasuressuchasincreasingpublicawareness,promotingsmoke-freeenvironments,andenhancingcleaningandventilationpracticesinindoorspaces.ThedevelopmentofeffectiveandaccessibletreatmentoptionsforTHS-relatedconditionsisalsoanimportantareaofresearch.
Overall,whilethereisstillmuchtolearnaboutthehealthimplicationsofTHS,itisclearthatthisisasignificantpublichealthconcernthatrequiresongoingattentionandaction.Asnewre
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