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
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
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DOI：
10.1016/j.jneuroim.2013.09.007
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发表时间：
2013-11-15
影响因子：
3.3
通讯作者：
Marques, Maria Julia
中科院分区：
文献类型：
--
作者：
de Carvalho, Samara Camacari;Apolinario, Leticia Montanholi;Marques, Maria Julia
在营养不良mdx小鼠和杜氏肌营养不良症中，炎症导致肌坏死。以前，我们证明了二十碳五烯酸（EPA）减少营养不良肌肉的炎症和坏死。在本研究中，我们研究了EPA和皮质激素deflazacort（DFZ）作为M1（iNOS表达细胞）和M2（CD 206表达细胞）巨噬细胞调节剂的作用。Mdx小鼠（14日龄）接受EPA或DFZ 16天。对膈肌、肱二头肌和股四头肌进行了研究。免疫荧光，免疫印迹和ELISA检测表明，EPA增加白细胞介素-10，减少干扰素-γ，更有效地比DFZ促进从M1到M2的转变。(C)2013爱思唯尔有限公司版权所有。
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-y and was more effective than DFZ in promoting a shift from M1 to M2. (C) 2013 Elsevier B.V. All rights reserved.