Inflammation in muscular dystrophy and the beneficial effects of non-steroidal anti-inflammatory drugs

被引:39
作者
Serra, Filippo [1 ]
Quarta, Marco [2 ,3 ]
Canato, Marta [4 ]
Toniolo, Luana [4 ]
De Arcangelis, Valeria [1 ]
Trotta, Attilio [1 ]
Spath, Lucia [1 ]
Monaco, Lucia [5 ]
Reggiani, Carlo [3 ,4 ]
Naro, Fabio [1 ,3 ]
机构
[1] Univ Roma La Sapienza, DAHFMO Unit Histol & Med Embryol, I-00161 Rome, Italy
[2] Stanford Univ, Dept Neurol & Neurol Sci, Sch Med, Stanford, CA 94305 USA
[3] IIM, Rome, Italy
[4] Univ Padua, Dept Human Anat & Physiol, Biophys Muscle Lab, Padua, Italy
[5] Univ Roma La Sapienza, Dept Physiol & Pharmacol, I-00161 Rome, Italy
关键词
COX; glucocorticoids; inflammation; muscular dystrophy; non-steroidal anti-inflammatory drugs; MOUSE DIAPHRAGM MUSCLE; SKELETAL-MUSCLE; MDX MICE; CONTRACTILE FUNCTION; DUCHENNE DYSTROPHY; ANIMAL-MODELS; PREDNISONE; EXPRESSION; PATHOLOGY; STRENGTH;
D O I
10.1002/mus.23432
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Introduction: Glucocorticoids are the only drugs available for the treatment of Duchenne muscular dystrophy (DMD), but it is unclear whether their efficacy is dependent on their anti-inflammatory activity. Methods: To address this issue, mdx mice were treated daily with methylprednisolone and non-steroidal anti-inflammatory drugs (NSAIDs: aspirin, ibuprofen, parecoxib). Results: NSAID treatment was effective in ameliorating muscle morphology and reducing macrophage infiltration and necrosis. The percentage of regenerating myofibers was not modified by the treatments. The drugs were effective in reducing COX-2 expression and inflammatory cytokines, but they did not affect utrophin levels. The effects of the treatments on contractile performance were analyzed. Isometric tension did not differ in treated and untreated muscle, but the resistance to fatigue was decreased by treatment with methylprednisolone and aspirin. Conclusions: NSAIDs have a beneficial effect on mdx muscle morphology, pointing to a crucial role of inflammation in the progression of DMD. Muscle Nerve, 2012
引用
收藏
页码:773 / 784
页数:12
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