Proteasome Inhibitor Bortezomib Ameliorates Intestinal Injury in Mice 英文参考文献.docVIP

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Proteasome Inhibitor Bortezomib Ameliorates Intestinal Injury in Mice 英文参考文献.doc

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Proteasome Inhibitor Bortezomib Ameliorates Intestinal Injury in Mice 英文参考文献

ProteasomeInhibitorBortezomibAmelioratesIntestinal InjuryinMice KoichiYanaba*,YoshihideAsano,YayoiTada,MakotoSugaya,TakafumiKadono,ShinichiSato DepartmentofDermatology,FacultyofMedicine,UniversityofTokyo,Tokyo,Japan Abstract Background: Bortezomib is a proteasome inhibitor that has shown impressive efficacy in the treatment of multiple myeloma.Inmice,theadditionofdextransulfatesodium(DSS)todrinkingwaterleadstoacutecolitisthatcanserveasan experimentalanimalmodelforhumanulcerativecolitis. Methodology/Principal Findings: Bortezomib treatment was shown to potently inhibit murine DSS-induced colitis. The attenuation of DSS-induced colitis was associated with decreased inflammatory cell infiltration in the colon. Specifically, + + bortezomib-treatedmiceshowedsignificantlydecreasednumbersofCD4 andCD8 Tcellsinthecolonandmesenteric lymph nodes. Bortezomib treatment significantly diminished interferon (IFN)-c expression in the colon and mesenteric lymph nodes. Furthermore, cytoplasmic IFN-c production by CD4+ and CD8+ T cells in mesenteric lymph nodes was substantially decreased by bortezomib treatment. Notably, bortezomib enhanced T cell apoptosis by inhibiting nuclear factor-kBactivationduringDSS-inducedcolitis. Conclusions/Significance:BortezomibtreatmentislikelytoinduceTcelldeath,therebysuppressingDSS-inducedcolitisby reducingIFN-cproduction. Citation:YanabaK,AsanoY,TadaY,SugayaM,KadonoT,etal.(2012)ProteasomeInhibitorBortezomibAmelioratesIntestinalInjuryinMice.PLoSONE7(3): e34587.doi:10.1371/journal.pone.0034587 Editor:LionelG.Filion,UniversityofOttawa,Canada ReceivedDecember27,2011;AcceptedMarch7,2012;PublishedMarch30,2012 Copyright: ? 2012 Yanaba et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding:ThisworkwassupportedbyagrantofResearchonIntractableDiseasesfromtheMinistryofHealth,Lab