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Nutritional intervention with cyanidin hinders the progression of muscular dystrophy

机译:用树花蛋白营养干预阻碍了肌营养不良的进展

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Muscular Dystrophies are severe genetic diseases due to mutations in structural genes, characterized by progressive muscle wasting that compromises patients' mobility and respiratory functions. Literature underlined oxidative stress and inflammation as key drivers of these pathologies. Interestingly among different myofiber classes, type I fibers display a milder dystrophic phenotype showing increased oxidative metabolism. This work shows the benefits of a cyanidin-enriched diet, that promotes muscle fiber-type switch and reduced inflammation in dystrophic alpha-sarcoglyan (Sgca) null mice having, as a net outcome, morphological and functional rescue. Notably, this benefit is achieved also when the diet is administered in dystrophic animals when the signs of the disease are seriously evident. Our work provides compelling evidence that a cyanidin-rich diet strongly delays the progression of muscular dystrophies, paving the way for a combinatorial approach where nutritional-based reduction of muscle inflammation and oxidative stress facilitate the successful perspectives of definitive treatments.
机译:由于结构基因的突变,肌肉营养不良是严重的遗传疾病,其特征在于促进患者的流动性和呼吸功能的渐进式肌肉浪费。文学强调氧化应激和炎症作为这些病理的关键驱动因素。有趣的是在不同的肌纤维类中,I型纤维显示较高的营养不良表型,显示出增加的氧化代谢。这项工作表明,富含花青蛋白的饮食的益处,促进肌纤维型开关和营养不良α-生气病(SGCA)无核小鼠的炎症,作为净结果,形态学和功能救援。值得注意的是,当患者在营养不良动物中施用时,当疾病的迹象严重明显时,这种益处也会实现。我们的作品提供了令​​人兴奋的证据表明,丰富的富含Cyanidin的饮食强烈延迟了肌营养不良的进展,为组合方法铺平了道路,其中基于肌肉炎症和氧化应激的营养型降低有助于定向治疗的成功视角。

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