大鼠血红素加氧酶-1表达对呼吸机相关性肺损伤时sod、mda的影响

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1、大鼠血红素加氧酶-1表达对呼吸机相关性肺损伤时SOD、MDA的影响【摘要】目的以大鼠呼吸机相关性肺损伤(VILI)为模型，用血晶素(hemin)诱导大鼠血红素加氧酶-1(HO-1)表达，观察VILI时超氧化物歧化酶(SOD)和丙二醛(MDA)活性变化及HO-1对SOD和MDA的影响，探讨在VILI过程中的抗氧化应激保护作用及其机制。方法32只雄性SD大鼠随机分成4组(每组n=8)：对照组只做气管切开术，保留自主呼吸;模型组气管切开后行机械通气4h;诱导剂组于模型制备前24h腹腔注射血晶素40μmol/kg;抑制剂组于模型制备前24h腹腔注射锌原卟啉(ZnPP)10μmol/kg。

2、机械通气4h后处死大鼠，收集肺组织和支气管肺泡灌洗液(BALF)标本，测定BALF中总蛋白含量，肺组织湿/干重比值(W/D)，肺组织LDH、SOD活性和MDA含量，检测肺组织HO-1蛋白表达，光镜下行肺组织病理学观察。结果与对照组相比，模型组大鼠肺组织病理损伤严重，肺W/D、BALF中总蛋白、LDH活性均明显增加，VILI模型复制成功。与模型组比较，诱导剂组肺组织HO-1表达增加，肺组织病理损伤明显减轻，SOD活性明显增加而MDA含量明显下降，用ZnPP抑制HO-1表达，此种保护作用消失。结论血晶素诱导大鼠HO-1表达可以增加SOD活性，降低MDA含量，减轻肺的氧化应激损伤，降低

3、VILI的程度。【关键词】呼吸机相关性肺损伤;血红素加氧酶-1;超氧化物歧化酶;丙二醛12　　Abstract:ObjectiveToobservethevariationsinsuperoxidedismutase(SOD)activityandmalondialdehyde(MDA)levelsinventilator-inducedlunginjury(VILI)andtheeffectsofHO-1expressiononSODandMDAwiththeestablishmentofratmodelofVILIandtheinductionofhemeoxygenase-

4、1expressionbyhemin,andtoinvestigatetheprotectiveeffectandtheunderlyingmechanismofanti-oxidativestressinVILI.Methods32maleSprague-Dawleyratswererandomizedinto4groups:controlgroup(tracheotomyonly,withspontaneousbreathingretained),modelgroup(tracheotomyfollowedby4hofmechanicalventilation),induce

5、rgroup(intraperitonealinjectionofhemin40μmol/kg24hbeforemodelestablishment),suppressorgroup(intraperitonealinjectionofZnPP10μmol/kg24hbeforemodelestablishment).4haftermechanicalventilation,theratsweresacrificedandthelungtissueandsamplesofbronchoalveolarlavagefluid(BALF)werecollectedfordetermi

6、nationoftotalproteininBALF,wet-to-dryweightratio(W/D)oflungs,LDHassayingandtheactivityofSODandMDAoflungtissue,detectionoflungtissueHO-1proteinexpression,andobservationofhistopathologicalchangesoflungsbylightmicroscopy.ResultsComparedwiththecontrol12group,ratsinthemodelgrouphadseriouslunghisto

7、pathologicalinjuryandmarkedincreaseinW/Doflungs,totalproteininBALFandLDHactivity,respectively,whichsuggestedthesuccessfulestablishmentofVILImodel.Intheinducergroup,ascomparedtothemodelgroup,HO-1expressionlevelincreasedandthelunghistopathologi