کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2525786 | 1119631 | 2008 | 9 صفحه PDF | دانلود رایگان |
Back groundMagnesium (Mg) deficiency may lead to serious metabolic, biological and organic dysfunctions, and cause various clinical disorders. In the current study, we explore endothelial cell activation, inflammation and cell death induced in the brain of adult mice by Mg-deficient diet.Methods and resultsNeither TNFα, substance P, sTNFRI, sTNFRII proteins (ELISA), nor TNFα, adherence molecules and prolactin mRNAs, nor NK1R (immunohistochemistry on brain sections) were up-regulated. No inflammatory infiltrates and no apoptotic cells were observed. Using cDNA assay, we showed a neuroprotective, anti-apoptotic and neurotrophic gene expression profile in the brain at early stage of hypomagnesemia. As a model for neuronal injury, mild sound stimulation of Mg-deficient mice without convulsive seizures triggers neither the release of substance P, nor the development of an inflammatory process or cell death in the brain.ConclusionOur results suggest that Mg-deficiency in mice favours the development of a neuroprotective environment in the brain.
Journal: Biomedicine & Pharmacotherapy - Volume 62, Issue 4, April–May 2008, Pages 264–272