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α-亚麻酸在 M1 样巨噬细胞中的抗炎作用与其增强 α-亚麻酸和亚油酸的氧化脂质生成有关。

Anti-inflammatory effects of α-linolenic acid in M1-like macrophages are associated with enhanced production of oxylipins from α-linolenic and linoleic acid.

机构信息

Department of Food and Human Nutritional Sciences, University of Manitoba, Canada; Canadian Centre for Agri-Food Research in Health and Medicine, Winnipeg, Canada.

Department of Food and Human Nutritional Sciences, University of Manitoba, Canada; Canadian Centre for Agri-Food Research in Health and Medicine, Winnipeg, Canada; Department of Physiology and Pathophysiology, University of Manitoba, Canada.

出版信息

J Nutr Biochem. 2018 Jul;57:121-129. doi: 10.1016/j.jnutbio.2018.03.020. Epub 2018 Apr 3.

Abstract

Chronic inflammation, mediated in large part by proinflammatory macrophage populations, contributes directly to the induction and perpetuation of metabolic diseases, including obesity, insulin resistance and type 2 diabetes. Polyunsaturated fatty acids (PUFAs) can have profound effects on inflammation through the formation of bioactive oxygenated metabolites called oxylipins. The objective of this study was to determine if exposure to the dietary omega-3 PUFA α-linolenic acid (ALA) can dampen the inflammatory properties of classically activated (M1-like) macrophages derived from the human THP-1 cell line and to examine the accompanying alterations in oxylipin secretion. We find that ALA treatment leads to a reduction in lipopolysaccharide (LPS)-induced interleukin (IL)-1β, IL-6 and tumor necrosis factor-α production. Although ALA is known to be converted to longer-chain PUFAs eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), DHA oxylipins were reduced overall by ALA treatment, as was LPS-induced secretion of EPA oxylipins. In contrast, we observed profound increases in oxylipins directly derived from ALA. Lipoxygenase products of linoleic acid were also dramatically increased, and LPS-induced production of AA oxylipins, particularly prostaglandin D2, was reduced. These results suggest that ALA may act to dampen the inflammatory phenotype of M1-like macrophages by a unique set of mechanisms distinct from those used by the long-chain omega-3 fatty acids EPA and DHA. Thus, there is strong rationale for investigating the functions of ALA oxylipins and lesser-known LA oxylipins since they hold promise as anti-inflammatory agents.

摘要

慢性炎症在很大程度上是由促炎巨噬细胞群介导的,它直接导致代谢性疾病的发生和持续,包括肥胖、胰岛素抵抗和 2 型糖尿病。多不饱和脂肪酸(PUFAs)可以通过形成称为氧化脂质的生物活性含氧代谢物对炎症产生深远影响。本研究的目的是确定暴露于膳食ω-3 多不饱和脂肪酸 α-亚麻酸(ALA)是否可以减弱源自人 THP-1 细胞系的经典激活(M1 样)巨噬细胞的炎症特性,并检查伴随的氧化脂质分泌的变化。我们发现,ALA 处理导致脂多糖(LPS)诱导的白细胞介素(IL)-1β、IL-6 和肿瘤坏死因子-α产生减少。尽管已知 ALA 会转化为更长链的多不饱和脂肪酸二十碳五烯酸(EPA)和二十二碳六烯酸(DHA),但 ALA 处理总体上降低了 DHA 氧化脂质,LPS 诱导的 EPA 氧化脂质分泌也降低了。相比之下,我们观察到源自 ALA 的氧化脂质明显增加。花生四烯酸的脂加氧酶产物也显著增加,LPS 诱导的 AA 氧化脂质产生,特别是前列腺素 D2,减少。这些结果表明,ALA 可能通过与长链 ω-3 脂肪酸 EPA 和 DHA 不同的独特机制来减弱 M1 样巨噬细胞的炎症表型。因此,强烈需要研究 ALA 氧化脂质和鲜为人知的 LA 氧化脂质的功能,因为它们有望成为抗炎剂。

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