Hardiman O, Brown R H, Beggs A H, Specht L, Sklar R M
Cecil B. Day Neuromuscular Research Laboratories, Massachusetts General Hospital, Charlestown.
Neurology. 1992 May;42(5):1085-91. doi: 10.1212/wnl.42.5.1085.
We report that the glucocorticoid methylprednisolone (Mepd) enhanced myogenesis in normal primary human muscle cultures, but inhibited myogenesis of most Duchenne/Becker muscle cultures. A decline in the magnitude of myogenic stimulation of Mepd correlated with age in a random group of control patients, including some with neurologic diseases other than Duchenne/Becker dystrophy. A case of Duchenne muscular dystrophy from an exceptionally young patient yielded a muscle culture that was myogenically stimulated by Mepd. These results suggest that continuous cycles of degeneration and regeneration of dystrophic muscle in vivo may result in a change of the glucocorticoid response of the muscle progenitor cells. The glucocorticoid effects suggest caution in the long-term clinical use of these agents for muscle disease such as Duchenne muscular dystrophy.
我们报告称，糖皮质激素甲泼尼龙（Mepd）在正常原代人肌肉培养物中增强了肌生成，但抑制了大多数杜兴氏/贝克氏肌肉培养物的肌生成。在一组随机的对照患者中，包括一些患有除杜兴氏/贝克氏营养不良之外的神经疾病的患者，Mepd对肌生成刺激的程度下降与年龄相关。一名来自异常年轻患者的杜兴氏肌营养不良病例产生了一种肌肉培养物，该培养物受到Mepd的肌生成刺激。这些结果表明，体内营养不良性肌肉的持续退化和再生循环可能导致肌肉祖细胞对糖皮质激素反应的改变。糖皮质激素的作用提示在长期临床使用这些药物治疗诸如杜兴氏肌营养不良等肌肉疾病时应谨慎。
