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1、ActaPhysiologicaSinica161Apr.1999,51(2),161～167ANTIPYRETICACTIONOFDEXAMETHASONEON3EGTAZICACID2INDUCEDFEVERINRABBITS33WANGHUA2DONG,WANGYAN2PING,LICHU2JIE,LUDA2XIANG,YANLIANG,QIREN2BIN(DepartmentofPathophysiology,MedicalCollegeofJinanUniversity,Guangzhou,510632)ABSTRACTThepurposeoftheprese
2、ntstudywastoinvestigatewhethertheantipyreticeffectofdexa2methasone(DEX)deliveredbyintravenousinjection(iv)onintracerebroventricularly(icv)administeredegtazicacid2inducedfebrileresponseisrelevanttothechangesincytosolicfreecalciumconcentrationofthehypothalamus.Thecolontemperaturesweremeasu
3、redbyathermistorandthecytosolicfreecalciumconcen22+tration([Ca]i)indissociatedbraincellswasmeasuredbyFura22AM.Theresultsdemonstratedthatthepyreticactionofegtazicacid(016μmol,icv)wasmarkedlyinhibitedbyDEX(5mg/kg,iv),butDEX(602+～120μmol/L)did′taffect[Ca]iindissociatedhypothalamuscells.Acti
4、nomycinD,whichinterfereswithgenetranscription(3nmol,icv),completelyabolishedtheantipyreticactionofDEXonegtazicacid2inducedfever.ThesefindingssuggestthattheantipyreticactionofDEXonegtazicacid2inducedfeverisrelatedtotheactivationofcertaingeneexpressioninthebrain,butnottothechangesoftransme
5、mbranecalciumioncurrentinhypothalamusneurons.Keywords:fever;egtazicacid;glucocorticoid;actinomycinD;calcium;dexamethasoneItiswellestablishedthatglucocorticoidshaveanantipyreticactiononfeverinducedbyavariety[1～3]ofpyrogens.However,cellularandmolecularmechanismsbywhichglucocorticoidsinhibi
6、tfeverhavenotbeenpreciselydefined.Althoughreductionoffeverbyglucocorticoidshasgenerallybeenat2[2～5]tributedtoinhibitionofcytokineandprostaglandin(PG)synthesis,theantipyreticeffectsofthese[3,6]glucocorticoidsontheresponsestoPGF2αandinterleukin28(IL28)andIL282inducedfeverisinde2[7]pendento
7、ftheactionofPGs.Ithasbeendemonstratedthatcorticotropinreleasinghormone(CRH)[8]mediatesthefebrileresponsestoIL26,IL28,IL21βandPGF2αandglucocorticoidseffectivelyinhibit[9]thesynthesisandreleaseofCRH,sothatantipyreticactionofglucocorticoidmayresultfrominhibi2[3]tionofsynthes
