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首页> 外文期刊>The Journal of Nutritional Biochemistry >Vitamin K suppresses the lipopolysaccharide-induced expression of inflammatory cytokines in cultured macrophage-like cells via the inhibition of the activation of nuclear factor kappa B through the repression of IKK alpha / beta phosphorylation.
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Vitamin K suppresses the lipopolysaccharide-induced expression of inflammatory cytokines in cultured macrophage-like cells via the inhibition of the activation of nuclear factor kappa B through the repression of IKK alpha / beta phosphorylation.

机译：维生素K通过抑制IKKα/β磷酸化来抑制核因子κB的活化，从而在培养的巨噬细胞样细胞中抑制脂多糖诱导的炎性细胞因子的表达。

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摘要

Vitamin K is essential for blood coagulation and bone metabolism in mammals. This vitamin functions as a cofactor in the posttranslational synthesis of gamma -carboxyglutamic acid (Gla) from glutamic acid residues. However, other functions of vitamin K have been reported recently. We previously found that vitamin K suppresses the inflammatory reaction induced by lipopolysaccharide (LPS) in rats and human macrophage-like THP-1 cells. In this study, we further investigated the mechanism underlying the anti-inflammatory effect of vitamin K by using cultures of LPS-treated human- and mouse-derived cells. All the vitamin K analogues analyzed in our study exhibited varied levels of anti-inflammatory activity. The isoprenyl side chain structures, except geranylgeraniol, of these analogues did not show such activity; warfarin did not interfere with this activity. The results of our study suggest that the 2-methyl-1,4-naphtoquinone ring structure contributes to express the anti-inflammatory activity, which is independent of the Gla formation activity of vitamin K. Furthermore, menaquinone-4, a form of vitamin K2, reduced the activation of nuclear factor kappa B (NF kappa B) and inhibited the phosphorylation of IKK alpha / beta after treatment of cells with LPS. These results clearly show that the anti-inflammatory activity of vitamin K is mediated via the inactivation of the NF kappa B signaling pathway.
机译：维生素K对于哺乳动物的凝血和骨骼代谢至关重要。该维生素在谷氨酸残基的γ-羧基谷氨酸（Gla）的翻译后合成中充当辅因子。然而，最近已经报道了维生素K的其他功能。我们以前发现维生素K抑制大鼠和人类巨噬细胞样THP-1细胞中脂多糖（LPS）诱导的炎症反应。在这项研究中，我们通过使用LPS处理的人和小鼠来源的细胞培养物，进一步研究了维生素K抗炎作用的潜在机制。在我们的研究中分析的所有维生素K类似物均表现出不同水平的抗炎活性。这些类似物，除了香叶基香叶醇以外，异戊二烯侧链结构均未显示出这种活性。华法林不干扰这种活性。我们的研究结果表明，2-甲基-1,4-萘醌环结构有助于表达抗炎活性，这与维生素K的Gla形成活性无关。此外，维生素E甲萘醌4 K 2 可以降低LPS处理细胞后核因子kappa B（NF kappa B）的活化并抑制IKK alpha /β的磷酸化。这些结果清楚地表明，维生素K的抗炎活性是通过NFκB信号通路的失活介导的。

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