- Auteur(s) : Hung-Chuan Pan, Meei-Ling Sheu, Hong-Lin Su, Ying-Ju Chen, Chun-Jung Chen, Dar-Yu Yang, Wen-Ta Chiu, Fu-Chou Cheng
, Department of Neurosurgery;, Stem Cell Center, Department of Medical Research, Taichung Veterans General Hospital, Taichung, Institute of Biomedical Sciences;, Institute of Life Sciences, National Chung-Hsing University, Taichung;, Department of Neurosurgery, Chang Bing Show Chwan Memorial Hospital, Changhua;, Department of Neurosurgery, Taipei Medical University, Shuang Ho Hospital, Taipei, Taiwan;
- Mots-clés : cytokines, inflammation, magnesium, nerve regeneration, sciatic nerve injury
- Page(s) : 54-70
- DOI : 10.1684/mrh.2011.0280
- Année de parution : 2011
Magnesium (Mg) supplements have been shown to significantly improve functional recovery in various neurological disorders. The essential benefits of Mg supplementation in peripheral nerve disorders have not been elucidated yet. The effect and mechanism of Mg supplementation on a sciatic nerve crush injury model was investigated. Sciatic nerve injury was induced in mice by crushing the left sciatic nerve. Mice were randomly divided into three groups with low-, basal- or high-Mg diets (corresponding to 10, 100 or 200% Mg of the basal diet). Neurobehavioral, electrophysiological and regeneration marker studies were conducted to explore nerve regeneration. First, a high Mg diet significantly increased plasma and nerve tissue Mg concentrations. In addition, Mg supplementation improved neurobehavioral, electrophysiological functions, enhanced regeneration marker, and reduced deposits of inflammatory cells as well as expression of inflammatory cytokines. Furthermore, reduced Schwann cell apoptosis was in line with the significant expression of bcl-2, bcl-X
L and down-regulated expression of active caspase-3 and cytochrome C. In summary, improved neurological function recovery and enhanced nerve regeneration were found in mice with a sciatic nerve injury that were fed a high- Mg diet, and Schwann cells may have been rescued from apoptosis by the suppression of inflammatory responses.