Associations between omega-3 fatty acid-derived lipid mediators and markers of inflammation in older subjects with low-grade chronic inflammation

老年低度慢性炎症患者体内ω-3脂肪酸衍生的脂质介质与炎症标志物之间的关联

阅读:1

Abstract

Cardiovascular disease (CVD), the leading cause of death in the United States and globally, is a chronic inflammatory disease likely caused by an impaired ability to resolve inflammation. Pre-clinical studies have provided strong evidence of the activating role of specialized pro-resolving lipid mediators (SPMs) derived from the omega-3 fatty acids eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA) and docosahexaenoic acid (DHA) on the resolution of inflammation. However, there is a dearth of information on the role of SPMs on inflammation in humans. Therefore, the aim of this study was to assess whether plasma concentrations of omega-3 fatty acids and their derived SPMs are associated with inflammatory markers in subjects with low-grade chronic inflammation (C-reactive protein >2 µg/mL). The plasma phospholipid content of omega-3 fatty acids, a marker of dietary intake, plasma concentrations of SPMs, and serum concentrations of inflammatory markers were measured in 21 older men and postmenopausal women (age 53-73 y) at the end of a four-week placebo phase (3 g/day high oleic acid sunflower oil). The phospholipid DHA content was inversely related to interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1) and IL-10 concentrations. Moreover, MCP-1 was inversely associated with the DHA-derived 14-HDHA and 4-HDHA, and IL-10 was inversely associated with EPA-derived 18-HEPE, 12-HEPE and 5-HEPE, DPA-derived Rv5(DPA), and DHA-derived 4-HDHA. These findings support the anti-inflammatory effect of dietary omega-3 fatty and suggest that lipid mediators derived from EPA, DPA, and DHA participate in the regulation of inflammation in subjects with chronic inflammation.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。