Fucoxanthin inhibits the inflammatory response by suppressing the activation of NF-κB and MAPKs in lipopolysaccharide-induced RAW 264 7 macrophages
Fucoxanthin inhibits the inflammatory response by suppressing the activation of NF-κB and MAPKs in lipopolysaccharide-induced RAW 264 7 macrophages
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DOI：
10.1016/j.ejphar.2010.09.032
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发表时间：
2010-12-15
影响因子：
5
通讯作者：
Jeon, You-Jin
中科院分区：
文献类型：
--
作者：
Kim, Kil-Nam;Heo, Soo-Jin;Jeon, You-Jin
一氧化氮合酶(NO)、前列腺素E-2(PGE(2))、肿瘤坏死因子(TNF)-α、白介素1-β(IL-1β)和白介素6(IL-6)等促炎介质参与了多种炎症性疾病的发病过程。本研究通过检测岩藻黄质(FX)对脂多糖(LPS)刺激的小鼠巨噬细胞RAW 264 7细胞FX诱导诱导型一氧化氮合酶(INOS)和环氧合酶(COX)水平的抑制作用，评价了FX的抗炎作用。-2(COX-2)蛋白及其伴随的NO和PGE生成的减少(2)此外，FX还抑制包括IL-1β、TNF-α和IL-6在内的炎性细胞因子的产生。此外，FX还抑制B(I Kappa B)α抑制物的细胞质降解和p50和p65蛋白的核转位，导致核因子kappaB的反式激活水平降低。此外，FX还显示出剂量依赖地抑制丝裂原活化蛋白激酶(MAPK)、JNK、ERK和p38的磷酸化水平。包括NO、PGE(2)、IL-1β、TNF-α和IL-6在内的促炎介质通过抑制RAW 264 7细胞中NF-kappa B的激活和MAPK的磷酸化，这些发现部分揭示了FX(C)2010 Elsevier BV抗炎特性的分子基础
It has been previously determined that pro-inflammatory mediators including nitric oxide (NO) prostaglandin E-2 (PGE(2)) tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta and IL 6 contribute to the courses of a variety of inflammatory diseases In this study we evaluated the anti inflammatory effects of fucoxanthin (FX) a natural biologically active substance isolated from Ishtge okamurae by determining its inhibitory effects on pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated murine macrophage RAW 264 7 cells FX induced dose-dependent reductions in the levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX 2) proteins and concomitant reductions in the production of NO and PGE(2) Additionally FX was shown to suppress the production of inflammatory cytokines including IL-1 beta TNF-alpha and IL-6 Furthermore FX inhibited the cytoplasmic degradation of inhibitors of B (I kappa B) alpha and the nuclear translocation of p50 and p65 proteins resulting in lower levels of nuclear factor (NF) kappa B transactivation Additionally FX was shown to induce a dose-dependent inhibition of the phosphorylation of mitogen activated protein kinases (MAPKs JNK ERK and p38) Collectively the results of this study demonstrate that FX reduces the levels of pro inflammatory mediators including NO PGE(2) IL 1 beta TNF-alpha and IL-6 via the inhibition of NF kappa B activation and the suppression of MAPK phosphorylation in RAW 264 7 cells These findings reveal in part the molecular basis underlying the anti-inflammatory properties of FX (C) 2010 Elsevier BV All rights reserved