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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

N-Acetylcysteine treatment reduces TNF-alpha levels and myonecrosis in diaphragm muscle of mdx mice

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Author(s):
Moraes Pinto, Rafael de Senzi [1] ; Ferretti, Renato [1] ; Rapucci Moraes, Luis Henrique [1] ; Neto, Humberto Santo [1] ; Marques, Maria Julia [1] ; Minatel, Elaine [1]
Total Authors: 6
Affiliation:
[1] Univ Estadual Campinas, UNICAMP, Inst Biol, Dept Biol Estrutural & Func, BR-13083970 Campinas, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Clinical Nutrition; v. 32, n. 3, p. 472-475, JUN 2013.
Web of Science Citations: 20
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-alpha), 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-alpha levels and protects the diaphragm muscle of mdx mice against necrosis. 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. Results: NAC reduced TNF-alpha and 4-HNE-protein adducts levels, inflammation, creatine kinase levels, and myonecrosis in diaphragm muscle. 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. (C) 2012 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved. (AU)

FAPESP's process: 10/01087-4 - In vivo and in vitro treatment, with N-acetylcistein and Deferoxamin in dystrophic mouse
Grantee:Luis Henrique Rapucci Moraes
Support type: Scholarships in Brazil - Doctorate