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Neuroprotective gene profile in the brain of magnesium-deficient mice
Michèle German-Fattal1, Florence Lecerf, Fadi Sabbagh
1Université Paris-Sud 11, Faculté de Pharmacie, Châtenay-Malabry Cedex F-92296, France. michele.german@u-psud.fr
Background:
Magnesium (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 Results:
Neither TNFalpha, substance P, sTNFRI, sTNFRII proteins (ELISA), nor TNFalpha, 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.
Conclusion:
Our results suggest that Mg-deficiency in mice favours the development of a neuroprotective environment in the brain.
Insights
Magnesium deficiency in mice did not cause brain inflammation or cell death. Instead, it surprisingly promoted a neuroprotective environment, even when exposed to mild neuronal injury.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Magnesium (Mg) deficiency can cause significant metabolic and organic dysfunctions.
- It is associated with various clinical disorders, highlighting the importance of Mg homeostasis.
- The brain's response to Mg deficiency, particularly concerning inflammation and cell death, requires further investigation.
Purpose of the Study:
- To investigate the effects of a magnesium-deficient diet on endothelial cell activation, inflammation, and cell death in the adult mouse brain.
- To determine if hypomagnesemia induces pro-inflammatory or pro-apoptotic changes in the brain.
Main Methods:
- Mice were fed a magnesium-deficient diet.
- Analysis of specific protein and mRNA levels related to inflammation (TNFalpha, substance P, adherence molecules, prolactin).
- Immunohistochemistry was used to detect NK1R expression.
- cDNA assays were performed to assess gene expression profiles.
- Neuronal injury was modeled using mild sound stimulation.
Main Results:
- No significant upregulation of TNFalpha, substance P, sTNFRI, sTNFRII proteins, or their corresponding mRNAs was observed.
- No inflammatory infiltrates or apoptotic cells were detected in the brain.
- cDNA analysis revealed a neuroprotective, anti-apoptotic, and neurotrophic gene expression profile in the early stages of hypomagnesemia.
- Mild sound stimulation did not trigger substance P release, inflammation, or cell death in Mg-deficient mice.
Conclusions:
- The study suggests that magnesium deficiency in mice does not induce brain inflammation or cell death.
- Instead, hypomagnesemia appears to foster a neuroprotective environment within the brain.
- This neuroprotective effect was observed even under conditions of mild neuronal injury.
