Burning magnesium, a sparkle in acute inflammation: gleams from experimental models, 2017

"...Conclusion
From the studies in vivo, ex vivo, and in vitro, it is clear that, under Mg deficiency, pro-inflammatory events predominate over its anti-inflammatory actions. Accordingly, physiologic or high extracellular concentrations of Mg exert anti-inflammatory properties. In cultured endothelial cells high Mg inhibits NF-kB and prevents the release of inflammatory mediators and cytokines [42], while in neutrophils and macrophages Mg inhibits oxidative burst [53, 54]. Moreover, high extracellular Mg reduces the release of inflammatory cytokines from leukocytes [55] and the levels of Toll-like receptor (TLR)4 in sebocytes [56]. Short-term exposure to Mg in vitro substantially reduced the frequency of neonatal monocytes producing TNF-a and IL-6 under constitutive and TLR-stimulated conditions, without influencing cell viability or phagocytic function. Upon TLR stimulation, Mg anti-inflammatory properties are due to the inhibition of NF-kB activation through the increase of IkBa levels [57]. It is likely that many of the effects of high Mg are due to its antagonisms with Ca and to its antioxidant action. Recently, Chandrasekaran and colleagues proposed a novel potential mechanism by which Mg inhibits inflammation. Mg could be involved in the activation of the thiamine pyrophosphate-dependent riboswitch, resulting in the increased synthesis from thiazole pyrophosphate of thiazole, which inhibits cyclooxygenase and hinders the formation of prostanoids [58].

This review underscores that there are many questions still open and highlights the need for more research to delineate a clear picture of how Mg, its transporters and sensors contribute to the modulation of acute inflammation..." http://www.jle.com/fr/revues/mrh/e-docs/burning_magnesium_a_sparkle_in_acute_inflammation_gleams_from_experimental_models_309488/article.phtml?tab=texte