Departamento de Biologia Estrutural e Funcional, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), Campinas, São Paulo 13083-970, Brazil.
J Neuroimmunol. 2013 Nov 15;264(1-2):41-7. doi: 10.1016/j.jneuroim.2013.09.007. Epub 2013 Sep 18.
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.
在营养不良型 mdx 小鼠和杜氏肌营养不良症中，炎症会导致肌肉坏死。此前，我们已经证明二十碳五烯酸（EPA）可以减少营养不良肌肉中的炎症和坏死。在本研究中，我们研究了 EPA 和皮质类固醇地夫可特（DFZ）作为 M1（表达 iNOS 的细胞）和 M2（表达 CD206 的细胞）巨噬细胞调节剂的作用。14 天大的 mdx 小鼠接受 EPA 或 DFZ 治疗 16 天。研究了膈肌、肱二头肌和股四头肌。免疫荧光、免疫印迹和 ELISA 检测表明，EPA 增加了白细胞介素 10，减少了干扰素-γ，并且比 DFZ 更有效地促进从 M1 向 M2 的转变。
