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牛磺酸氯胺抑制脂多糖诱导的RAW 264.7巨噬细胞中的葡萄糖摄取及葡萄糖转运蛋白1表达。

Taurine chloramine inhibits LPS-induced glucose uptake and glucose transporter 1 expression in RAW 264.7 macropages.

作者信息

Kim Chaekyun, Kim Seongtag

机构信息

Laboratory for Leukocyte Signaling Research, and Center for Advanced Medical Education by BK21 Project, Inha University School of Medicine, Incheon, Korea.

出版信息

Adv Exp Med Biol. 2009;643:473-80.

PMID:19239179
Abstract

Inflammatory cells use glucose as a primary source of metabolic energy, and thus increased uptake of glucose and high rates of glycolysis are characteristics of inflamed cells. Taurine chloramine (TauCl) is the product of a reaction between cellular taurine and hypochlorous acid (HOCl/OCl-), the latter produced by the halide-dependent myeloperoxidase (MPO) system in inflammatory cells. Taurine, a major metabolite of cysteine, protects cells from inflammatory injury by removing toxic hypochlorous acid formed by the MPO system, and also by inhibiting the production of inflammatory mediators. In the present study, we examined the effect of TauCl on glucose uptake and the expression of the glucose transporter 1 (GLUT1) in RAW 264.7 murine macrophages stimulated with lipopolysaccharide (LPS). Glucose uptake was measured by employing labeled glucose analogue [18F]-2-fluoro-2-deoxy-D-glucose (FDG). Stimulation RAW 264.7 cells with LPS increased glucose uptake and led to an upregulation in GLUT1 expression, effects that were abrogated in macrophages treated with TauCl. These data suggest that TauCl can inhibit LPS-mediated enhancement of glucose uptake through inhibition of the upregulation of glucose transporter expression in activated macrophages. This represents one of the mechanisms by which TauCl modulates inflammatory cell function.

摘要

炎症细胞将葡萄糖作为代谢能量的主要来源,因此葡萄糖摄取增加和糖酵解速率加快是炎症细胞的特征。牛磺酸氯胺(TauCl)是细胞内牛磺酸与次氯酸(HOCl/OCl-)反应的产物,后者由炎症细胞中依赖卤化物的髓过氧化物酶(MPO)系统产生。牛磺酸是半胱氨酸的主要代谢产物,它通过清除MPO系统形成的有毒次氯酸以及抑制炎症介质的产生来保护细胞免受炎症损伤。在本研究中,我们检测了TauCl对脂多糖(LPS)刺激的RAW 264.7小鼠巨噬细胞中葡萄糖摄取及葡萄糖转运蛋白1(GLUT1)表达的影响。通过使用标记的葡萄糖类似物[18F]-2-氟-2-脱氧-D-葡萄糖(FDG)来测量葡萄糖摄取。用LPS刺激RAW 264.7细胞可增加葡萄糖摄取并导致GLUT1表达上调,而在用TauCl处理的巨噬细胞中这些效应被消除。这些数据表明,TauCl可通过抑制活化巨噬细胞中葡萄糖转运蛋白表达的上调来抑制LPS介导的葡萄糖摄取增强。这代表了TauCl调节炎症细胞功能的机制之一。

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