dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorde Carvalho, Samara Camaçari
dc.creatorApolinário, Leticia Montanholi
dc.creatorMatheus, Selma Maria Michelin
dc.creatorSanto Neto, Humberto
dc.creatorMarques, Maria Julia
dc.date2014-05-27T11:30:47Z
dc.date2016-10-25T18:54:37Z
dc.date2014-05-27T11:30:47Z
dc.date2016-10-25T18:54:37Z
dc.date2013-10-01
dc.date.accessioned2017-04-06T02:40:32Z
dc.date.available2017-04-06T02:40:32Z
dc.identifierJournal of Neuroimmunology.
dc.identifier0165-5728
dc.identifier1872-8421
dc.identifierhttp://hdl.handle.net/11449/76713
dc.identifierhttp://acervodigital.unesp.br/handle/11449/76713
dc.identifier10.1016/j.jneuroim.2013.09.007
dc.identifierWOS:000327567700006
dc.identifier2-s2.0-84884600034
dc.identifierhttp://dx.doi.org/10.1016/j.jneuroim.2013.09.007
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/897404
dc.descriptionIn dystrophic mdx mice and in Duchenne muscular dystrophy, inflammation contributes to myonecrosis. Previously, we demonstrated that eicosapentaenoic acid (EPA) decreased inflammation and necrosis in dystrophic muscle. In the present study, we examined the effects of EPA and the corticoid deflazacort (DFZ) as modulators of M1 (iNOS-expressing cells) and M2 (CD206-expressing cells) macrophages. Mdx mice (14 days old) received EPA or DFZ for 16 days. The diaphragm, biceps brachii and quadriceps muscles were studied. Immunofluorescence, immunoblotting and ELISA assays showed that EPA increased interleucin-10, reduced interferon-γ and was more effective than DFZ in promoting a shift from M1 to M2. © 2013 Elsevier B.V. All rights reserved.
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.languageeng
dc.relationJournal of Neuroimmunology
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectDeflazacort
dc.subjectDystrophy
dc.subjectEPA
dc.subjectInflammation
dc.subjectM1 macrophages
dc.subjectM2 macrophages
dc.titleEPA protects against muscle damage in the mdx mouse model of Duchenne muscular dystrophy by promoting a shift from the M1 to M2 macrophage phenotype
dc.typeOtro


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