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饮食中海鱼油替代物改变莱姆病感染小鼠踝关节中环氧化酶产物谱。

Dietary fish oil substitution alters the eicosanoid profile in ankle joints of mice during Lyme infection.

机构信息

Departments of Chemistry, Biochemistry, and Pharmacology, University of California, San Diego, La Jolla, CA, USA.

出版信息

J Nutr. 2012 Aug;142(8):1582-9. doi: 10.3945/jn.112.157883. Epub 2012 Jun 13.

Abstract

Dietary ingestion of (n-3) PUFA alters the production of eicosanoids and can suppress chronic inflammatory and autoimmune diseases. The extent of changes in eicosanoid production during an infection of mice fed a diet high in (n-3) PUFA, however, has not, to our knowledge, been reported. We fed mice a diet containing either 18% by weight soybean oil (SO) or a mixture with fish oil (FO), FO:SO (4:1 ratio), for 2 wk and then infected them with Borrelia burgdorferi. We used an MS-based lipidomics approach and quantified changes in eicosanoid production during Lyme arthritis development over 21 d. B. burgdorferi infection induced a robust production of prostanoids, mono-hydroxylated metabolites, and epoxide-containing metabolites, with 103 eicosanoids detected of the 139 monitored. In addition to temporal and compositional changes in the eicosanoid profile, dietary FO substitution increased the accumulation of 15-deoxy PGJ(2), an antiinflammatory metabolite derived from arachidonic acid. Chiral analysis of the mono-hydroxylated metabolites revealed they were generated from primarily nonenzymatic mechanisms. Although dietary FO substitution reduced the production of inflammatory (n-6) fatty acid-derived eicosanoids, no change in the host inflammatory response or development of disease was detected.

摘要

饮食摄入(n-3)多不饱和脂肪酸会改变类二十烷酸的产生,并能抑制慢性炎症和自身免疫性疾病。然而,据我们所知,在高(n-3)多不饱和脂肪酸饮食喂养的感染小鼠中,类二十烷酸产生的变化程度尚未有报道。我们用含有 18%重量大豆油(SO)或鱼油(FO)混合物的饮食(FO:SO 为 4:1 比例)喂养小鼠 2 周,然后用伯氏疏螺旋体感染它们。我们使用基于 MS 的脂质组学方法,定量分析了莱姆关节炎发展过程中类二十烷酸产生的变化,时间跨度为 21 天。B. burgdorferi 感染诱导了前列腺素、单羟基代谢物和含环氧化物代谢物的大量产生,在监测的 139 种代谢物中有 103 种被检测到。除了类二十烷酸谱的时间和组成变化外,FO 替代饮食增加了抗炎代谢物 15-脱氧 PGJ(2)的积累,该代谢物来源于花生四烯酸。单羟基代谢物的手性分析表明它们主要是通过非酶机制生成的。尽管 FO 替代饮食减少了炎症(n-6)脂肪酸衍生的类二十烷酸的产生,但未检测到宿主炎症反应或疾病发展的变化。

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