BACKGROUND:Brainischemiainvolvessecondaryinflammation,whichsignificantlycontributestotheoutcomeofischemicinsults.Vascularendothelialgrowthfactor(VEGF)mayplayanimportantroleinthevascularresponsetocerebralischemia,becauseischemiastimulatesVEGFexpressioninthebrain,andVEGFpromotesformationofnewcerebralbloodvessels.Minocycline,atetracyclinederivative,protectsagainstcerebralischemiaandreducesinflammation,oxidativestress,andapoptosis.OBJECTIVE:ToobservetheinfluenceofminocyclineonVEGF,interleukin-1beta(IL-1β),andtumornecrosisfactoralpha(TNF-α)expressioninWistarratswithfocalcerebralischemia/reperfusioninjury,andtostudytheneuroprotectionmechanismofminocyclineagainstfocalcerebralischemia/reperfusioninjury.DESIGN,TIMEANDSETTING:Randomized,controlledexperiment,whichwasperformedintheChongqingKeyLaboratoryofNeurologybetweenMarch2007andMarch2008.MATERIALS:Atotalof36female,Wistarratsunderwentsurgerytoinsertathreadintotheleftmiddlecerebralartery.Animalswererandomlypidedintosham-operation,minocyclinetreatment,andischemia/reperfusiongroups,with12ratsineachgroup.Minocycline(HuishiPharmaceuticalLimitedCompany,China)wasdissolvedto0.5g/Linnormalsaline.METHODS:A0.5-1.0cmthreadwasinsertedintoratsfromthesham-operationgroup.Ratsintheischemia/reperfusiongroupunderwentischemiaandreperfusion.Theminocyclinegroupreceivedminocycline(50mg/kg)12and24hoursfollowingischemiaandreperfusion,whereastheothergroupsreceivedsalineatthecorrespondingtimepoints.MAINOUTCOMEMEASURES:mRNAandproteinexpressionofIL-1βandTNF-αwasmeasuredbyreversetranscriptase-polymerasechainreaction(RT-PCR)andenzymelinkedimmunosorbentassay(ELISA),respectively.VEGFmRNAandproteinexpressionwasexaminedbyRT-PCR,Westernblot,andELISA.RESULTS:Minocyclinedecreasedthefocalinfarctvolume.VEGF,IL-1β,andTNF-αexpressionw
