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J Neuroimmunol. 2013 Nov 15;264(1-2):41-7. doi: 10.1016/j.jneuroim.2013.09.007. Epub 2013 Sep 18.

EPA protects against muscle damage in the mdx mouse model of Duchenne muscular dystrophy by promoting a shift from the M1 to M2 macrophage phenotype.

Author information

1
Departamento de Biologia Estrutural e Funcional, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), Campinas, São Paulo 13083-970, Brazil.

Abstract

In 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.

KEYWORDS:

Deflazacort; Dystrophy; EPA; Inflammation; M1 macrophages; M2 macrophages

PMID:
24090650
DOI:
10.1016/j.jneuroim.2013.09.007
[Indexed for MEDLINE]

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