Departamento de Anatomia, Biologia Celular, Fisiologia e Biofísica, Instituto de Biologia, Universidade Estadual de Campinas, Campinas, São Paulo 13083-970, Brazil.
J Neuroimmunol. 2011 Mar;232(1-2):145-50. doi: 10.1016/j.jneuroim.2010.10.032. Epub 2010 Dec 4.
In dystrophin-deficient fibers of mdx mice and in Duchenne muscular dystrophy, inflammation and increased production of tumor necrosis factor alpha (TNF-α) contribute to myonecrosis. We examined the effects of eicosapentaenoic acid (EPA) on dystrophic muscle degeneration. Mdx mice (14 days old) received EPA for 16 days. The sternomastoid, diaphragm and biceps brachii muscles were removed. Control mdx mice received vehicle. EPA decreased creatine kinase and myonecrosis and reduced the levels of TNF-α. These results suggest that EPA plays a protective role in dystrophic muscle degeneration, possibly by reducing TNF-α, and support further investigations of EPA as a potential therapy for dystrophinopathies.
在 mdx 小鼠的营养不良肌纤维和杜氏肌营养不良症中，炎症和肿瘤坏死因子-α（TNF-α）的增加导致肌肉坏死。我们研究了二十碳五烯酸（EPA）对营养不良性肌肉退化的影响。14 天大的 mdx 小鼠接受 EPA 治疗 16 天。取出胸锁乳突肌、膈肌和肱二头肌。对照 mdx 小鼠接受载体。EPA 降低肌酸激酶和肌肉坏死，并降低 TNF-α的水平。这些结果表明，EPA 通过减少 TNF-α在营养不良性肌肉退化中发挥保护作用，并支持进一步研究 EPA 作为治疗营养不良性肌病的潜在疗法。
