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来自硅藻的岩藻黄质醇可改善脂多糖刺激的 BV-2 小胶质细胞中的神经炎症反应。

Fucoxanthinol from the Diatom Ameliorates Neuroinflammatory Responses in Lipopolysaccharide-Stimulated BV-2 Microglia.

机构信息

Institute for Food and Bioresource Engineering, College of Engineering, Peking University, Beijing 100871, China.

Institute for Advanced Study, Shenzhen University, Shenzhen 518060, China.

出版信息

Mar Drugs. 2020 Feb 17;18(2):116. doi: 10.3390/md18020116.

DOI:10.3390/md18020116
PMID:32079242
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7074591/
Abstract

In recent years, microalgae have drawn increasing attention as a valuable source of functional food ingredients. Intriguingly, is rich in fucoxanthinol that is seldom found in natural sources. Fucoxanthinol, a marine xanthophyll carotenoid, possesses various beneficial bioactivities. Nevertheless, it's not clear whether fucoxanthinol could exert anti-neuroinflammatory function. In light of these premises, the aim of the present study was to investigate the anti-inflammatory role of fucoxanthinol purified from in Lipopolysaccharide (LPS)-stimulated microglia. The results showed that pre-treatment of fucoxanthinol remarkably attenuated the expression of LPS-induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and the production of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), prostaglandin E2 (PGE-2), nitric oxide (NO) and reactive oxygen species (ROS) induction. Modulation mechanism studies revealed that fucoxanthinol hampered nuclear factor-kappa B (NF-κB), Akt, and mitogen-activated protein kinase (MAPK) pathways. Meanwhile, fucoxanthinol led to the enhancement of nuclear translocation of NF-E2-related factor 2 (Nrf2), and the upregulation of heme oxygenase-1 (HO-1) and NAD(P)H: quinone oxidoreductase 1 (NQO-1). Taken together, the results indicated that fucoxanthinol obtained from had great potential as a neuroprotective agent in neuroinflammation and neurodegenerative disorders.

摘要

近年来,微藻作为功能性食品成分的宝贵来源受到了越来越多的关注。有趣的是, 富含很少在天然来源中发现的岩藻黄质醇。岩藻黄质醇是一种海洋类胡萝卜素叶黄素,具有多种有益的生物活性。然而,目前尚不清楚岩藻黄质醇是否具有抗炎作用。鉴于这些前提,本研究旨在研究从 中纯化的岩藻黄质醇对脂多糖 (LPS) 刺激的小胶质细胞的抗炎作用。结果表明,岩藻黄质醇预处理可显著减弱 LPS 诱导的一氧化氮合酶 (iNOS) 和环氧化酶-2 (COX-2) 的表达,以及肿瘤坏死因子-α (TNF-α)、白细胞介素-6 (IL-6)、前列腺素 E2 (PGE-2)、一氧化氮 (NO) 和活性氧 (ROS) 的产生。调节机制研究表明,岩藻黄质醇阻碍了核因子-κB (NF-κB)、Akt 和丝裂原活化蛋白激酶 (MAPK) 途径。同时,岩藻黄质醇导致核因子 E2 相关因子 2 (Nrf2) 的核易位增强,并上调血红素加氧酶-1 (HO-1) 和 NAD(P)H:醌氧化还原酶 1 (NQO-1)。综上所述,这些结果表明, 中提取的岩藻黄质醇作为神经炎症和神经退行性疾病的神经保护剂具有巨大潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/2b52e55873dc/marinedrugs-18-00116-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/db250be79c2c/marinedrugs-18-00116-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/d6ab86270043/marinedrugs-18-00116-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/cc21edd40a84/marinedrugs-18-00116-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/c3e621638622/marinedrugs-18-00116-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/78960ee510c9/marinedrugs-18-00116-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/ba1a08cf2fb5/marinedrugs-18-00116-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/2b52e55873dc/marinedrugs-18-00116-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/db250be79c2c/marinedrugs-18-00116-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/d6ab86270043/marinedrugs-18-00116-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/cc21edd40a84/marinedrugs-18-00116-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/c3e621638622/marinedrugs-18-00116-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/78960ee510c9/marinedrugs-18-00116-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/ba1a08cf2fb5/marinedrugs-18-00116-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7764/7074591/2b52e55873dc/marinedrugs-18-00116-g007a.jpg

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