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.
© 2013.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Analysis of Variance
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Animals
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Antigens, Differentiation / metabolism
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Creatine Kinase / blood
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Disease Models, Animal
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Eicosapentaenoic Acid / therapeutic use*
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Enzyme-Linked Immunosorbent Assay
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Female
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Interferon-gamma / metabolism
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Interleukin-10 / metabolism
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Lectins, C-Type / metabolism
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Macrophages / drug effects*
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Macrophages / metabolism
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Male
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Mannose Receptor
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Mannose-Binding Lectins / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Inbred mdx
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Muscles / drug effects*
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Muscles / pathology
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Muscular Dystrophy, Duchenne / drug therapy*
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Muscular Dystrophy, Duchenne / genetics
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Muscular Dystrophy, Duchenne / pathology*
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Nitric Oxide Synthase Type II / metabolism
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Phenotype*
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Pregnenediones / therapeutic use
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Receptors, Cell Surface / metabolism
Substances
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Antigens, Differentiation
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Lectins, C-Type
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Mannose Receptor
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Mannose-Binding Lectins
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Pregnenediones
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Receptors, Cell Surface
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monocyte-macrophage differentiation antigen
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Interleukin-10
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Interferon-gamma
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Eicosapentaenoic Acid
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Nitric Oxide Synthase Type II
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Creatine Kinase
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deflazacort