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Vitamin E treatment decreases muscle injury in mdx mice.
- Source :
-
Nutrition (Burbank, Los Angeles County, Calif.) [Nutrition] 2017 Nov - Dec; Vol. 43-44, pp. 39-46. Date of Electronic Publication: 2017 Jul 13. - Publication Year :
- 2017
-
Abstract
- Objective: Oxidative stress, in addition to the absence of the dystrophin protein, has been considered an important regulator of Duchenne muscular dystrophy (DMD). Vitamin E presents an important role as a potent antioxidant and in preserving the integrity of the cell membrane. In this study, we evaluated the effects of vitamin E therapy on some physiological pathways that can contribute to muscle injury in the diaphragm muscle of mdx mice (the experimental model of DMD) such as CK levels, inflammatory response, oxidative stress, and the enzymatic antioxidant system.<br />Methods: Mdx mice (14 d old) received 40 mg vitamin E/kg daily by oral gavage for 14 d, followed by the removal of the diaphragm muscle. Control mdx mice and C57BL/10 mice received saline only for the same period and were used as controls.<br />Results: Vitamin E reduced the muscle fiber damage, oxidative stress, and inflammation process in the diaphragm muscle of mdx mice.<br />Conclusions: Vitamin E improves skeletal muscle injury in mdx mice, promoting membrane repair and exhibiting antioxidant and antiinflammatory effects. These vitamin E effects suggest that this antioxidant therapy may be a relevant approach for dystrophinopathies.<br /> (Copyright © 2017 Elsevier Inc. All rights reserved.)
- Subjects :
- Animals
Diaphragm pathology
Disease Models, Animal
Dystrophin deficiency
Female
Inflammation drug therapy
Male
Mice
Mice, Inbred C57BL
Mice, Inbred mdx
Muscular Dystrophy, Duchenne drug therapy
Oxidative Stress drug effects
Antioxidants administration & dosage
Muscle, Skeletal pathology
Muscular Dystrophy, Duchenne pathology
Vitamin E administration & dosage
Subjects
Details
- Language :
- English
- ISSN :
- 1873-1244
- Volume :
- 43-44
- Database :
- MEDLINE
- Journal :
- Nutrition (Burbank, Los Angeles County, Calif.)
- Publication Type :
- Academic Journal
- Accession number :
- 28935143
- Full Text :
- https://doi.org/10.1016/j.nut.2017.07.003