Prednisone can protect against exercise-induced muscle damage
Prednisone can protect against exercise-induced muscle damage
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DOI：
10.1007/bf00869001
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发表时间：
1996-05-01
影响因子：
6
通讯作者：
Wokke, JHJ
中科院分区：
文献类型：
--
作者：
Jacobs, SCJM;Bootsma, AL;Wokke, JHJ
在实验动物运动模型中，我们测试了每天给予泼尼松是否能防止机械诱导的肌纤维损伤的发展。用不同剂量的泼尼松（每天1至50 mg/kg体重）或安慰剂治疗6周龄大鼠8天。在治疗的第6天，大鼠被迫在水平跑步机上跑步2小时。运动后两天，比目鱼肌的形态学损伤进行了量化，使用光学显微镜和半自动图像分析系统。在运动前（第5天）和运动后立即（第6天）测量肌酸激酶（CK）活性。用蛋白质印迹法研究了安慰剂组和每天接受5 mg泼尼松/kg体重并进行和不进行运动的组中肌营养不良蛋白的表达。用抗快速肌球蛋白抗体测定泼尼松对纤维类型分布的影响，并用溴脱氧尿苷（BrdU）免疫组织化学研究泼尼松对肌肉卫星细胞增殖活性的影响。肌肉纤维损伤呈剂量依赖性。在安慰剂组中，平均（SEM）受损肌纤维面积为4%（1%）。接受低剂量泼尼松（每天1或2.5 mg/kg）的组显示出相似的肌肉损伤水平。然而，使用5 mg泼尼松/kg/天，肌纤维损伤量[平均值（SEM）]显著降低至1.4%（0.5%）（P小于或等于0.05，Student t检验）。大剂量强的松对脑损伤无保护作用。除了每天接受50 mg泼尼松/kg体重的组外，运动后CK活性直接增加两倍。蛋白质印迹光密度分析后，未发现抗肌萎缩蛋白的量发生变化。强的松不影响纤维分布和卫星细胞标记指数。我们的结论是，泼尼松，给予适当的剂量，保护肌纤维免受机械损伤的发展，可能是通过稳定肌纤维膜，这种行动可以解释泼尼松的有益效果观察杜氏肌营养不良症患者。
Ln an experimental animal exercise model we tested whether daily administration of prednisone prevents the development of mechanically induced muscle fibre damage. Six-week-old rats were treated with different doses of prednisone ranging from 1 to 50 mg/kg body weight per day or with placebo, for 8 days. On day 6 of treatment the rats were forced to run for 2 h on a level treadmill. Two days after exercise morphological damage in the soleus muscles was quantified using light microscopy and a semi-automatic image analysis system. Creatine kinase (CK) activity was measured before exercise (day 5) and directly after exercise (day 6). The expression of dystrophin in a placebo group and in a group that received 5 mg prednisone/kg body weight per day with and without performing exercise was studied with Western blotting. The effect of prednisone on fibre type distribution was determined with an antibody against fast myosin and the effect of prednisone on the proliferative activity of muscle satellite cells was studied using bromodeoxyuridine (BrdU) immunohistochemistry. Exercise-induced muscle fibre damage varied in a dose-dependent way. In the placebo group the mean (SEM) damaged muscle fibre area was 4% (1%). The groups that received low doses of prednisone, 1 or 2.5 mg/kg per day, showed a similar level of muscle damage. However, with 5 mg prednisone/kg per day the amount of muscle fibre damage [mean (SEM)] was significantly reduced to 1.4% (0.5%) (P less than or equal to 0.05, Student's t-test). High doses of prednisone had no protective effect. Directly after exercise the CK activity was increased two-fold, except in the group that received 50 mg prednisone/kg body weight per day. No changes in the amount of dystrophin were found after densitometric analysis of the Western blots. Prednisone did not affect the fibre distribution or the labelling index of satellite cells. We conclude that prednisone, given in an appropriate dose, protects muscle fibres against the development of mechanically induced damage, possibly by stabilizing the muscle fibre membranes, This action may explain the beneficial effect of prednisone observed in Duchenne muscular dystrophy patients.