Abstract:objectivetostudyofTNFalphaGhrelinhumanbrainmicrovascularendothelialcellsinduced(HBMEC)mononuclearcellschemotaxisprotein1(MCP-1),TNFalphagrouptojoindifferentconcentrationTNFalpha;GhrelinpretreatmentsectionfirstjoinGhrelinpretreatment1h,-PCRmethodtodetectMCP-1mRNAlevel,immuneimprintingmethodtodetectp38phosphorylation(p-p38),MCP-1mRNAexpressobviousenhancement,andtheconcentrationofacertaindose-responserelationship(P<)inthecytoplasmandP-p38proteinexpressionalsosignificantlyincreased(P<).GhrelinpretreatmentcanreduceMCP-1mRNAcytoplasmandthep-p38proteinexpression(p<).ConclusionGhrelinmayinhibitp-p38pathwaysinhibitTNFalphamediatedHBMECMCP-:mononuclearcellschemotaxisprotein1;Thehumanbrainmicrovascularendothelialcells;GhrelinInrecentyears,andtherelationshipbetweenGhrelininflammationispaidattentionto,butforinflammation,Ghrelinindifferenttissuesfunctionisnotthesame,needtomakeclearfurther[1~5].April2008toJuly2009,westudiedGhrelinTNFalphainductionofthehumanbrainmicrovascularendothelialcells(HBMEC)mononuclearcellschemotaxisprotein1(MCP-1)phosphorylationmRNAandp38(p-p38)theinfluenceoftheexpression,thispaperdiscussesGhre-Lininthepossibleanti-inflammatorymechanismvessel,asGhrelinappliedtoclinicaldiabetescerebrovasculardiseaseandprovidedther
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