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Anti-Prion Activity of Brilliant Blue G 英文参考文献
Anti-PrionActivityofBrilliantBlueG
YoshifumiIwamaru1.,TakatoTakenouchi2.,YuichiMurayama1,HiroyukiOkada1,MorikazuImamura1,
YoshihisaShimizu1,MakotoHashimoto3,ShirouMohri1,TakashiYokoyama1,HiroshiKitani2*
1Prion Disease Research Center, National Institute of Animal Health, Tsukuba, Ibaraki, Japan, 2Animal Immune and Cell Biology Research Unit, National Institute of
AgrobiologicalSciences,Tsukuba,Ibaraki,Japan,3DivisionofSensoryandMotorSystems,TokyoMetropolitanInstituteofMedicalScience,Setagaya-ku,Tokyo,Japan
Abstract
Background: Prion diseases are fatal neurodegenerative disorders with no effective therapy currently available.
Accumulatingevidencehasimplicatedover-activationofP2X7ionotropicpurinergicreceptor(P2X7R)intheprogression
ofneuronallossinseveralneurodegenerativediseases.Thishasledtothespeculationthatsimultaneousblockadeofthis
receptorandprionreplicationcanbeaneffectivetherapeuticstrategyforpriondiseases.WehavefocusedonBrilliantBlue
G (BBG), a well-known P2X7R antagonist, possessing a chemical structure expected to confer anti-prion activity and
examineditsinhibitoryeffectontheaccumulationofpathogenicisoformsofprionprotein(PrPres)inacellularandamouse
modelofpriondiseaseinordertodetermineitstherapeuticpotential.
PrincipalFindings:BBGpreventedPrPresaccumulationininfectedMG20microglialandN2aneuralcellsat50%inhibitory
concentrations of 14.6 and 3.2mM, respectively. Administration of BBG in vivo also reduced PrPres accumulation in the
brainsofmicewithpriondisease.However,itdidnotappeartoalleviatethediseaseprogressioncomparedtothevehicle-
treatedcontrols,implyingacomplexroleofP2X7Rontheneuronaldegenerationinpriondiseases.
Significance: These results provide novel insights into the pathophysiology of prion diseases and have important
implicationsforthetreatment.
Citation:IwamaruY,TakenouchiT,MurayamaY,OkadaH,ImamuraM,etal.(2012)Anti-PrionActivityofBrilliantBlueG.PLoSONE7(5):e37896.doi:10.1371/
journal.pone.0037896
Editor:CorinneIdaLasmezas,TheScrippsResearchInstitut
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