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N-acetylcysteine treatment reduces TNF-α levels and myonecrosis in diaphragm muscle of mdx mice.
- Source :
-
Clinical nutrition (Edinburgh, Scotland) [Clin Nutr] 2013 Jun; Vol. 32 (3), pp. 472-5. Date of Electronic Publication: 2012 Jun 23. - Publication Year :
- 2013
-
Abstract
- Background & Aims: Duchenne muscular dystrophy (DMD) is a genetic muscle disease caused by the absence of dystrophin. An established animal model of DMD is the mdx mouse, which is unable to express dystrophin. Inflammation, particularly the proinflammatory cytokine tumor necrosis factor alpha (TNF-α), strongly contributes to necrosis in the dystrophin-deficient fibers of the mdx mice and in DMD. In this study we investigated whether the antioxidant N-acetylcysteine (NAC) decreases TNF-α levels and protects the diaphragm muscle of mdx mice against necrosis.<br />Methods: Mdx mice (14 days old) received daily intraperitoneal injections of NAC for 14 days, followed by removal of the diaphragm muscle. Control mdx mice were injected with saline.<br />Results: NAC reduced TNF-α and 4-HNE-protein adducts levels, inflammation, creatine kinase levels, and myonecrosis in diaphragm muscle.<br />Conclusions: NAC may be used as a complementary treatment for dystrophinopathies. However, clinical trials are needed to determine the appropriate dose for patients with Duchenne muscular dystrophy.<br /> (Copyright © 2012 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.)
- Subjects :
- Animals
Antioxidants therapeutic use
Diaphragm pathology
Dystrophin deficiency
Dystrophin genetics
Inflammation drug therapy
Inflammation pathology
Mice
Mice, Inbred C57BL
Mice, Inbred mdx
Muscle, Skeletal pathology
Necrosis pathology
Acetylcysteine therapeutic use
Diaphragm drug effects
Muscle, Skeletal drug effects
Necrosis drug therapy
Tumor Necrosis Factor-alpha blood
Subjects
Details
- Language :
- English
- ISSN :
- 1532-1983
- Volume :
- 32
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Clinical nutrition (Edinburgh, Scotland)
- Publication Type :
- Academic Journal
- Accession number :
- 22727548
- Full Text :
- https://doi.org/10.1016/j.clnu.2012.06.001