Cannabinoid Agonists Inhibit Neuropathic Pain Induced by Brachial Plexus Avulsion in Mice by Affecting Glial Cells and MAP Kinases 英文参考文献.docVIP

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Cannabinoid Agonists Inhibit Neuropathic Pain Induced by Brachial Plexus Avulsion in Mice by Affecting Glial Cells and MAP Kinases 英文参考文献.doc

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Cannabinoid Agonists Inhibit Neuropathic Pain Induced by Brachial Plexus Avulsion in Mice by Affecting Glial Cells and MAP Kinases 英文参考文献

CannabinoidAgonistsInhibitNeuropathicPainInduced byBrachialPlexusAvulsioninMicebyAffectingGlial CellsandMAPKinases AnaF.Paszcuk1,RafaelC.Dutra1,KathrynA.B.S.daSilva1,NaraL.M.Quinta?o2,MariaM.Campos3, Joa?oB.Calixto1* 1DepartmentofPharmacology,CentreofBiologicalSciences,UniversidadeFederaldeSantaCatarina,Floriano′polis,SantaCatarina,Brazil,2ProgramadeMestradoem Cie?nciasFarmace?uticas,UniversidadedoValedeItaja?′,Itaja?′,Brazil,3SchoolofDentistryandInstituteofToxicology,Pontif?′ciaUniversidadeCato′licadoRioGrandedoSul, PortoAlegre,Brazil Abstract Background:Manystudieshaveshowntheantinociceptiveeffectsofcannabinoid(CB)agonistsindifferentmodelsofpain. Herein,wehaveinvestigatedtheirrelevanceinneuropathicpaininducedbybrachialplexusavulsion(BPA)inmice. Methodology/PrincipalFindings:MiceunderwentBPAorshamsurgery.ThemRNAlevelsandproteinexpressionofCB1 and CB2 receptors were assessed by RT-PCR and immunohistochemistry, respectively. The activation of glial cells, MAP kinases and transcription factors were evaluated by immunohistochemistry. The antinociceptive properties induced by cannabinoidagonistswereassessedonthe5thand30thdaysaftersurgery.WeobservedamarkedincreaseinCB1andCB2 receptormRNAandproteinexpressioninthespinalcordanddorsalrootganglion,eitheratthe5thor30thdayaftersurgery. BPA also induced a marked activation of p38 and JNK MAP kinases (on the 30th day), glial cells, such as microglia and astrocytes,andthetranscriptionfactorsCREBandNF-kB(atthe5thand30thdays)inthespinalcord.Systemictreatment with cannabinoid agonists reduced mechanical allodynia on both the 5th and 30th days after surgery, but the greatest resultswereobservedbyusingcentralroutesofadministration,especiallyatthe30th day.TreatmentwithWIN55,212-2 preventedtheactivationofbothglialcellsandMAPkinases,associatedwithanenhancementofCREBandNF-k Bactivation. Conclusions/Significance:OurresultsindicatearelevantroleforcannabinoidagonistsinBPA,reinforcingtheirpotential therapeuticrelevanceforthemanagement