Beneficial Effects of Ethyl Pyruvate through Inhibiting High-Mobility Group Box 1 Expression and TLR4NF- B Pathway after Traumatic Brain Injury in the Rat英文文献资料.docVIP

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Beneficial Effects of Ethyl Pyruvate through Inhibiting High-Mobility Group Box 1 Expression and TLR4NF- B Pathway after Traumatic Brain Injury in the Rat英文文献资料.doc

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Beneficial Effects of Ethyl Pyruvate through Inhibiting High-Mobility Group Box 1 Expression and TLR4NF- B Pathway after Traumatic Brain Injury in the Rat英文文献资料

HindawiPublishingCorporation MediatorsofIn?ammation Volume2011,ArticleID807142,10pages doi:10.1155/2011/807142 ResearchArticle Bene?cialEffectsofEthylPyruvatethroughInhibiting High-MobilityGroupBox1ExpressionandTLR4/NF-κ BPathway afterTraumaticBrainInjuryintheRat XingfenSu,HandongWang,JinbingZhao,HaoPan,andLeiMao DepartmentofNeurosurgery,JinlingHospital,SchoolofMedicine,NanjingUniversity,305EastZhongshanRoad,JiangsuProvince, Nanjing210002,China CorrespondenceshouldbeaddressedtoHandongWang,hdwangnj@ Received17January2011;Accepted21March2011 AcademicEditor:T?aniaSilviaFr¨ode Copyright?2011XingfenSuetal.ThisisanopenaccessarticledistributedundertheCreativeCommonsAttributionLicense, whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperlycited. Ethylpyruvate(EP)hasdemonstratedneuroprotectivee?ectsagainstacutebraininjurythroughitsanti-in?ammatoryaction.The nuclearproteinhigh-mobilitygroupbox1(HMGB1)canactivatein?ammatorypathwayswhenreleasedfromdyingcells.This studywasdesignedtoinvestigatetheprotectivee?ectsofEPagainstsecondarybraininjuryinratsafterTraumaticBrainInjury (TBI).Adultmaleratswererandomlydividedintothreegroups:(1)Sham+vehiclegroup,(2)TBI+vehiclegroup,and(3)TBI +EPgroup(n=30pergroup).Rightparietalcorticalcontusionwasmadebyusingaweight-droppingTBImethod.InTBI+EP group,EPwasadministeredintraperitoneallyatadosageof75mg/kgat5min,1and6hafterTBI.Brainsampleswereharvested at24hafterTBI.WefoundthatEPtreatmentmarkedlyinhibitedtheexpressionsofHMGB1andTLR4,NF-κBDNAbinding activityandin?ammatorymediators,suchasIL-1β,TNF-αandIL-6.Also,EPtreatmentsigni?cantlyamelioratedbeamwalking performance,brainedema,andcorticalapoptoticcelldeath.Theseresultssuggestthattheprotectivee?ectsofEPmaybemediated bythereductionofHMGB1/TLR4/NF-κB-mediatedin?ammatoryresponseintheinjuredratbrain. 1.Introduction passivelyreleasedfromthenecroticcellsotherthanapoptotic cells,andthentriggersin?ammation[7,8].Recently,much evidence identi?es HMGB1 as a cytokin