John Libbey Eurotext

Magnesium Research

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Magnesium deficiency heightens lipopolysaccharide-induced inflammation and enhances monocyte adhesion in human umbilical vein endothelial cells Volume 31, numéro 2, April-May-June 2018

Illustrations

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Tableaux

Auteurs
1 Department of Nutrition and Food Science, Princess Nora Bint Abdulrahman University, Kingdom of Saudi Arabia
2 Division of Nutritional Sciences, School of Biosciences, The University of Nottingham, United Kingdom
* Correspondence: SC Langley-Evans, School of Biosciences, University of Nottingham, Sutton Bonington Campus, Loughborough, LE12 5RD, United Kingdom
  • Mots-clés : Magnesium, endothelial cell, adhesion molecule, cytokines
  • DOI : 10.1684/mrh.2018.0436
  • Page(s) : 39-48
  • Année de parution : 2018

Given a possible anti-inflammatory role of magnesium in endothelial cells, the aim of this study was to investigate the effects of magnesium on human umbilical vein endothelial cell (HUVEC) viability, gene expression, and the pro-inflammatory response caused by a bacterial endotoxin (LPS). HUVECs were cultured at three different concentrations of magnesium sulphate (0.1 mM; control-1 mM; 5 mM) for 72 hours. Exposing the cells to LPS reduced cell viability in culture with low magnesium, but high magnesium protected the HUVECs from LPS-induced cell death. LPS-treated HUVECs cultured in low magnesium showed up-regulation of mRNA expression for pro-inflammatory factors and the expression of cytokine proteins, including IL-2, IL-3, IL-8, IL-15 and MCP-1. This was associated with greater adhesion of monocytes to the cells. In contrast, high magnesium decreased the expression of inflammatory factors and cytokines. The study found that LPS activation of the expression of many pro-inflammatory factors is exacerbated in the presence of low magnesium concentration whilst a high magnesium concentration partly inhibited the inflammatory response to LPS.