Krahn M J, Anderson J E
Department of Anatomy, University of Manitoba, Winnipeg, Canada.
J Neurol Sci. 1994 Sep;125(2):138-46. doi: 10.1016/0022-510x(94)90026-4.
In order to study whether myofiber size is an important determinant of the severity of dystrophic injury, mdx and control mice were treated with an anabolic steroid, nandrolone decanoate, for 3 weeks. Treatment resulted in a population of significantly smaller fibers in both strains, and was accompanied by an increase in the proportionate area or the number of foci of dystrophic injury in mdx soleus (slow-twitch) or tibialis anterior plus extensor digitorum longus (fast-twitch) muscles, respectively. As well, serum creatine kinase activity was increased in steroid-treated mdx mice. Fiber centronucleation, an index of accumulated injury and repair, in steroid-treated mdx soleus was doubled compared to that observed in soleus muscles from untreated mdx mice. There was no change in the distribution of immunoreactive basic fibroblast growth factor, important in muscle cell proliferation, with the increased damage from treatment. However, presumptive muscle precursor cells (identified by immunoperoxidase histochemistry for neural cell adhesion molecule), appeared to be more abundant in foci of very recent fiber damage in muscles from steroid-treated than untreated mdx mice. Results show that mdx dystrophy is worsened by anabolic steroid treatment, possibly by altered influences on muscle use patterns and muscle precursor fusion, and is not accompanied by an increase in fiber size.
为了研究肌纤维大小是否是营养不良性损伤严重程度的重要决定因素，对mdx小鼠和对照小鼠用合成代谢类固醇癸酸诺龙治疗3周。治疗导致两种品系中均出现一群明显更小的纤维，并且在mdx比目鱼肌（慢肌）或胫前肌加趾长伸肌（快肌）中，分别伴随着营养不良性损伤病灶的相对面积或数量增加。同样，经类固醇治疗的mdx小鼠血清肌酸激酶活性升高。在经类固醇治疗的mdx比目鱼肌中，作为累积损伤和修复指标的纤维中心核化，相比于未经治疗的mdx小鼠比目鱼肌中观察到的情况增加了一倍。在治疗导致损伤增加的情况下，对肌肉细胞增殖很重要的免疫反应性碱性成纤维细胞生长因子的分布没有变化。然而，在经类固醇治疗的mdx小鼠肌肉中，与未经治疗的mdx小鼠相比，在最近发生纤维损伤的病灶中，推测的肌肉前体细胞（通过神经细胞粘附分子的免疫过氧化物酶组织化学鉴定）似乎更为丰富。结果表明，合成代谢类固醇治疗会使mdx营养不良恶化，可能是通过改变对肌肉使用模式和肌肉前体细胞融合的影响，并且不会伴随着纤维大小的增加。
