The Anti-Inflammatory Effect of Algae-Derived Lipid Extracts on Lipopolysaccharide (LPS)-Stimulated Human THP-1 Macrophages.
The Anti-Inflammatory Effect of Algae-Derived Lipid Extracts on Lipopolysaccharide (LPS)-Stimulated Human THP-1 Macrophages.
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DOI：
10.3390/md13085402
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发表时间：
2015-08-20
期刊：
影响因子：
5.4
通讯作者：
Stanton C
中科院分区：
文献类型：
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作者：
Robertson RC;Guihéneuf F;Bahar B;Schmid M;Stengel DB;Fitzgerald GF;Ross RP;Stanton C
藻类含有大量的抗炎生物活性化合物，如omega-3多不饱和脂肪酸(n-3 PUFA)和叶绿素a，因此，作为饮食成分，它们的提取物可能对心血管疾病等慢性炎症相关的代谢性疾病有效。本研究用脂多糖(LPS)刺激人THP-1巨噬细胞，研究了三种红藻(紫菜、棕榈藻和角叉菜)和一种微藻(Pavlova Lutheri)的脂类提取物的抗炎作用。提取物含有34%-42%的n-3多不饱和脂肪酸和5%-7%的粗提取物作为色素，包括叶绿素a、β-胡萝卜素和岩藻黄质。手掌侧柏脂提取物可抑制THP-1细胞产生促炎细胞因子IL-6(p<；0.05)和IL-8(p<；0.05)，而灯盏细辛则抑制IL-6(p<；0.01)的产生。对一组与炎症信号通路相关的92个基因的定量基因表达分析显示，脂类提取物下调了14个促炎基因(TLR1、TLR2、TLR4、TLR8、TRAF5、TRAF6、TNFSF18、IL6R、IL23、CCR1、CCR4、CCL17、STAT3、MAP3K1)的表达。脂类提取物可有效抑制Toll样受体、趋化因子和活化B细胞核因子轻链增强剂(NF-κB)信号分子介导的内毒素诱导的促炎信号转导通路。这些结果表明，紫云英、棕榈云杉、白云英和皱纹云杉的脂类提取物能抑制脂多糖诱导的人巨噬细胞的炎症反应。因此，藻类脂类提取物作为慢性炎症相关代谢性疾病的抗炎成分值得进一步开发。
Algae contain a number of anti-inflammatory bioactive compounds such as omega-3 polyunsaturated fatty acids (n-3 PUFA) and chlorophyll a, hence as dietary ingredients, their extracts may be effective in chronic inflammation-linked metabolic diseases such as cardiovascular disease. In this study, anti-inflammatory potential of lipid extracts from three red seaweeds (Porphyra dioica, Palmaria palmata and Chondrus crispus) and one microalga (Pavlova lutheri) were assessed in lipopolysaccharide (LPS)-stimulated human THP-1 macrophages. Extracts contained 34%–42% total fatty acids as n-3 PUFA and 5%–7% crude extract as pigments, including chlorophyll a, β-carotene and fucoxanthin. Pretreatment of the THP-1 cells with lipid extract from P. palmata inhibited production of the pro-inflammatory cytokines interleukin (IL)-6 (p < 0.05) and IL-8 (p < 0.05) while that of P. lutheri inhibited IL-6 (p < 0.01) production. Quantitative gene expression analysis of a panel of 92 genes linked to inflammatory signaling pathway revealed down-regulation of the expression of 14 pro-inflammatory genes (TLR1, TLR2, TLR4, TLR8, TRAF5, TRAF6, TNFSF18, IL6R, IL23, CCR1, CCR4, CCL17, STAT3, MAP3K1) by the lipid extracts. The lipid extracts effectively inhibited the LPS-induced pro-inflammatory signaling pathways mediated via toll-like receptors, chemokines and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling molecules. These results suggest that lipid extracts from P. lutheri, P. palmata, P. dioica and C. crispus can inhibit LPS-induced inflammatory pathways in human macrophages. Therefore, algal lipid extracts should be further explored as anti-inflammatory ingredients for chronic inflammation-linked metabolic diseases.