首页> 外文OA文献 >Fucofuroeckol-A fromEisenia bicyclisInhibits Inflammation in Lipopolysaccharide-Induced Mouse Macrophages via Downregulation of the MAPK/NF-κB Signaling Pathway
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Fucofuroeckol-A fromEisenia bicyclisInhibits Inflammation in Lipopolysaccharide-Induced Mouse Macrophages via Downregulation of the MAPK/NF-κB Signaling Pathway

机译:Fucofuroeckol-a Fromeisenia bicyclisiNigates通过MAPK / NF-κB信号通路的下调,通过下调脂多糖诱导的小鼠巨噬细胞炎症

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摘要

Fucofuroeckol-A (FF) isolated from an edible perennial brown seaweed Eisenia bicyclis was shown to be potent anti-inflammatory agents. FF suppressed the production of nitric oxide (NO) and prostaglandin E2 (PGE2) and the expression of inducible nitric oxide synthase and cyclooxygenase-2 dose dependently in lipopolysaccharide- (LPS-) induced RAW 264.7 mouse macrophages. An enzyme-linked immunosorbent assay and cytometric bead array assay demonstrated that FF significantly reduced the production of proinflammatory cytokines, such as interleukin-6 and tumor necrosis factor-α, and that of the monocyte chemoattractant protein-1. Moreover, FF reduced the activation of nuclear factor κB (NF-κB) and mitogen-activated protein kinases (MAPKs). These results strongly suggest that the inhibitory effects of fucofuroeckol-A from E. bicyclis on LPS-induced NO and PGE2 production might be due to the suppression of the NF-κB and MAPK signaling pathway.
机译:从可食用的多年生棕海藻类艾西哥亚洲雌激素中分离出的Fucofuroeckol-A(FF)是有效的抗炎剂。 FF抑制了一氧化氮(NO)和前列腺素E2(PGE2)的产生,以及依赖于脂多糖 - (LPS-)诱导的原料264.7小鼠巨噬细胞的诱导型一氧化氮合酶和环氧氧酶-2剂量的表达。酶联免疫吸附测定和细胞晶珠阵列测定证明,FF显着降低了促炎细胞因子的产生,例如白细胞介素-6和肿瘤坏死因子-α,以及单核细胞化学蛋白-1的产生。此外,FF降低了核因子κB(NF-κB)和丝裂原激活蛋白激酶(MAPK)的激活。这些结果强烈表明,Fucofurockol-A来自E.的抑制作用来自E.的LPS诱导的NO和PGE2产生可能是由于NF-κB和MAPK信号通路的抑制。

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