摘要
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
出版日期
2006年03月13日（中国Betway体育网页登陆平台首次上网日期，不代表论文的发表时间）
