α-甲基泼尼松龙可促进肌营养不良蛋白缺陷型和对照小鼠培养物中的骨骼肌生成。

alpha-Methylprednisolone promotes skeletal myogenesis in dystrophin-deficient and control mouse cultures.

作者信息

Metzinger L, Passaquin A C, Warter J M, Poindron P

机构信息

Département d'Immunologie, Immunopharmacologie et Pathologie, Université Louis Pasteur, Illkirch, France.

出版信息

Neurosci Lett. 1993 Jun 11;155(2):171-4. doi: 10.1016/0304-3940(93)90700-u.

DOI:10.1016/0304-3940(93)90700-u

PMID:8377947

Abstract

We have examined the influence of the glucocorticoid alpha-methylprednisolone (PDN) on the morphological differentiation of skeletal muscle cells derived from dystrophin-deficient C57BL/10 mdx, congenic C57BL/10 and allogenic Balb/c newborn mice. We show that PDN enhances myogenic cell numbers in dystrophin-deficient cultures as well as in matched controls. A parallel increase in the fusion rate of myoblasts into myotubes occurs while the size of myotubes, as determined by nuclei per myotube, is slightly increased. This promoting effect of PDN on myogenesis could be related to the enhanced muscular function observed in PDN-treated Duchenne's muscular dystrophy-affected boys.

摘要

我们研究了糖皮质激素α-甲基泼尼松龙（PDN）对来自肌营养不良蛋白缺陷的C57BL/10 mdx、同基因C57BL/10和异基因Balb/c新生小鼠的骨骼肌细胞形态分化的影响。我们发现，PDN可增加肌营养不良蛋白缺陷培养物以及匹配对照组中的成肌细胞数量。同时，成肌细胞融合为肌管的速率平行增加，而根据每个肌管中的细胞核数量确定的肌管大小略有增加。PDN对肌生成的这种促进作用可能与在接受PDN治疗的杜氏肌营养不良症男孩中观察到的肌肉功能增强有关。