| Full text | |
| Author(s): |
Mauricio, Adriana Fogagnolo
[1]
;
Minatel, Elaine
[1]
;
Santo Neto, Humberto
[1]
;
Marques, Maria Julia
[1]
Total Authors: 4
|
| Affiliation: | [1] Univ Estadual Campinas UNICAMP, Dept Biol Estrut & Func, Inst Biol, BR-13083970 Campinas, SP - Brazil
Total Affiliations: 1
|
| Document type: | Journal article |
| Source: | Clinical Nutrition; v. 32, n. 4, p. 636-642, AUG 2013. |
| Web of Science Citations: | 18 |
| Abstract | |
Background Ea aims: In Duchenne muscular dystrophy (DMD) and in the mdx mouse model of DMD, the lack of dystrophin leads to muscle degeneration and inflammation contributes to progression of the disease. In this study, we evaluated the effects of commercially available fish oil containing EPA and docosahexaenoic acid (DHA) on mdx. Methods: Mdx mice (14 days old) were treated with fish oil (FDC Vitamins; 0.002 g EPA and 0.001 g DHA) for 16 days by gavage. Control mdx mice received mineral oil (Nujol). Grip strength measurement was used for functional evaluation. The stemomastoid, diaphragm and biceps brachii muscles were removed and processed for histopathology and Western blot analysis. Results: Fish oil decreased creatine kinase and myonecrosis. In all muscles studied, the inflammatory area was significantly reduced after treatment (18.0 +/- 3.0% inflammatory area in untreated mdx mice versus 4.0 +/- 1% in treated mdx mice). Fish oil protected against the loss of muscle strength. Fish oil significantly reduced the levels of TNF-alpha and the levels of 4-HNE-protein adducts (30-34% reduction for both) in all muscles studied. Conclusions: Commercially available fish oil may be potentially useful to ameliorate dystrophic progression of skeletal muscles, deserving further clinical trials in DMD patients. (C) 2012 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved. (AU) | |
| FAPESP's process: | 11/02474-4 - Treatment in vivo and in vitro with calcium blocker and antioxidant in mdx mice |
| Grantee: | Elaine Minatel |
| Support type: | Regular Research Grants |