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Exacerbated immune stress response during experimental magnesium deficiency results from abnormal cell calcium homeostasis.

机译:实验性镁缺乏期间加剧的免疫应激反应是由异常的细胞钙稳态引起的。

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摘要

The aim of this study was to assess the potential mechanism underlying the enhanced inflammatory processes during magnesium deficit. In this study, exacerbated response to live bacteria and platelet activating factors was shown in rats fed a magnesium-deficient diet. Peritoneal cells from these animals also showed enhanced superoxide anion production and calcium mobilising potency following in vitro stimulation. The latter effect occurred very early in the course of magnesium deficiency. These studies first showed that an abnormal calcium handling induced by extracellular magnesium depression in vivo may be at the origin of exacerbated inflammatory response.
机译:这项研究的目的是评估镁缺乏时炎症过程增强的潜在机制。在这项研究中,饲喂缺镁饮食的大鼠表现出对活细菌和血小板活化因子的加剧反应。在体外刺激后,这些动物的腹膜细胞还显示出增强的超氧阴离子产生和钙动员能力。后者的影响很早就发生在镁缺乏的过程中。这些研究首先表明,体内细胞外镁抑制引起的异常钙处理可能是炎症反应加剧的起源。

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