米诺环素对大鼠脑缺血再灌注后nf-κb、iκbα和tnf-α表达的影响

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1、AbstractneuroprotectivemechanismofMinocycline．Materialandmethods72healthyadultS-DratswererandomlydividedintotheSham—operatedgroup(Sham)，ischemia-reperfusiongroup(IR)andMCtreatmentgroup(MT)．ThemodelofIntraluminalThreadOcclusionModelwasestablishedaccordingtoZeaLongxsmethodafteraadvisableimprovement．T

2、heoperationofShamgroupWastreatedjustthesameastheothertwogroupsbesideswithouttheinsertionthread．MinocyclineWasdeliveredbyintragastricadministrationafterreperfusion(firstdoseWas45mg／kg，others22．5mg／kgevery12h)，andbotllTheShamgroupandIRgroupweredeliveredphysiologicalsalineatthesametimepointuntiltheywe

3、resacrificed．ThebrainhistopathologyWasobservedat48hafterreperfusionbyH—Estaining．WedetectedneuronapoptosisbyTUNELtoevaluatetheischemia-reperfusioninjuryandtheneuroprotectiveeffectofminocyeline．TheexpressionofIrBa、NF—xBp65andTNF-awerefurtherdetectedbyimmunohistochemistrytoobservethevariationandtheef

4、fectsofminocycline．Results(1)ComparedwiththeIRgroup，thepathologicalchangeofbraintissueWasobviouslyrelievedaftercerebralischemia-reperfusion48h；(2)ComparedwiththeIRgroup，theneuronapoptosiswassignificantlydecreasedintheMTgroupaftercerebralischemia-reperfusion48h；(3)TheexpressionofNF-rBp65positivecell

5、shasincreasedsignificantlyafterreperfusion6handapproachthemaxon24h，thenithasslightlydecreaseon48h．TheexpressionofTNF·apositivecellshasincreasedsignificantlyafterreperfusion6handapproachthemaxon24h，thenitstillkeepahighlevelon48h．Ontheaccordingtimepoint，thepositivecellnumbersofNF-rd3p65orTNF-ainIRgro

6、upweresignificantlyhigherthantheShamgroup(P

7、ons(1)nleexpressionofIrBaWaSdecreasedbutNF一加p65Wasover-expressedinratsafterFocalCerebralIschemia-Reperfusion．(2)MCcanincreaseTheexpressionofIxBabutdeceasetheexpressionofNF-加p65andTNF一％MCplayaneuroprotective