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Neoagaro-oligosaccharide monomers inhibit inflammation in LPS-stimulated macrophages through suppression of MAPK and NF-κB pathways

机译:新糖寡糖单体通过抑制MAPK和NF-κB途径抑制LPS刺激的巨噬细胞的炎症

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摘要

Neoagaro-oligosaccharides derived from agarose have been demonstrated to possess a variety of biological activities, such as anti-bacteria and anti-oxidative activities. In this study, we mainly explored the inhibitory effects and the mechanisms of neoagaro-oligosaccharide monomers against LPS-induced inflammatory responses in mouse macrophage RAW264.7 cells. The results indicated that neoagaro-oligosaccharide monomers especially neoagarotetraose could significantly reduce the production and release of NO in LPS-induced macrophages. Neoagarotetraose significantly suppressed the expression and secretion of inducible nitric oxide synthase (iNOS) and proinflammatory cytokines such as TNF-α and IL-6. The inhibition mechanisms may be associated with the inhibition of the activation of p38MAPK, Ras/MEK/ERK and NF-κB signaling pathways. Thus, neoagarotetraose may attenuate the inflammatory responses through downregulating the MAPK and NF-κB signaling pathways in LPS-stimulated macrophages. In summary, the marine-derived neoagaro-oligosaccharide monomers merit further investigation as novel anti-inflammation agents in the future.
机译:已经证明衍生自琼脂糖的新琼脂寡糖具有多种生物活性,例如抗细菌和抗氧化活性。在这项研究中,我们主要探讨了新琼脂寡糖单体对LPS诱导的小鼠巨噬细胞RAW264.7细胞炎症反应的抑制作用和机制。结果表明,新琼脂糖寡糖单体,特别是新琼脂糖四糖可以显着降低LPS诱导的巨噬细胞中NO的产生和释放。新琼脂四糖显着抑制诱导型一氧化氮合酶(iNOS)和促炎细胞因子(如TNF-α和IL-6)的表达和分泌。抑制机制可能与抑制p38MAPK,Ras / MEK / ERK和NF-κB信号通路的激活有关。因此,新琼脂四糖可能通过下调LPS刺激的巨噬细胞中的MAPK和NF-κB信号通路来减轻炎症反应。总之,海洋来源的新琼脂寡糖单体作为未来的新型消炎剂值得进一步研究。

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