新琼寡糖单体通过抑制 MAPK 和 NF-κB 通路抑制 LPS 刺激的巨噬细胞炎症。
Neoagaro-oligosaccharide monomers inhibit inflammation in LPS-stimulated macrophages through suppression of MAPK and NF-κB pathways.
机构信息
College of Food Science and Engineering, and School of Medicine and Pharmacy, Ocean University of China, Qingdao, 266003, China.
Institute of Cerebrovascular Diseases, Affiliated Hospital of Qingdao University Medical College, Qingdao, 266003, China.
出版信息
Sci Rep. 2017 Mar 7;7:44252. doi: 10.1038/srep44252.
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.
从琼脂衍生的新琼寡糖已被证明具有多种生物活性，如抗菌和抗氧化活性。在这项研究中，我们主要探讨了新琼寡糖单体对 LPS 诱导的小鼠巨噬细胞 RAW264.7 细胞炎症反应的抑制作用及其机制。结果表明，新琼寡糖单体，特别是新琼四糖，可显著降低 LPS 诱导的巨噬细胞中 NO 的产生和释放。新琼四糖显著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，海洋来源的新琼寡糖单体作为新型抗炎剂值得进一步研究。
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