急性炎症模型中促炎/促炎脂质介质的差异分析

Lopez-Gaydon Amandine, Baillif Vincent, B. Cindy, Van Goethem Emeline, Demarne Frédéric, Dubourdeau Marc, B. Nicolas
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引用次数: 0

摘要

致编辑:来自多不饱和脂肪酸(PUFA)的生物活性脂质介质通过对炎症和免疫反应的精细和时空控制,有助于皮肤健康[1]。花生四烯酸;20:4n-6),二十碳五烯酸(EPA;20:5n-3)和二十二碳六烯酸(DHA;22:6n-3)是人体皮肤中最主要的必需脂肪酸[2]。它们是合成促炎介质的前体,或主动结束这一过程,并因其特定作用而命名为专门的促炎脂质介质(SPMs)。在诱导炎症消退后,最初触发炎症的细胞经历生化范式转变,称为“脂质介质类转换”,在此期间,它们停止产生经典的促炎介质,并开始积极合成SPMs。这些包括aa衍生的脂毒素(LXA4和LXB4), epa衍生的溶解蛋白和dha衍生的溶解蛋白,保护和蛋白[3]。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Differential Profile of Proinflammatory/Proresolving Lipid Mediators in Acute Inflammation Model using Young and Old Skin Biopsies
To the Editor, Bioactive lipid mediators derived from polyunsaturated fatty acids (PUFA) contribute to skin health through a fine and a spatiotemporal control of inflammation and immune response [1]. Arachidonic acid (AA; 20:4n-6), eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3) are the most predominant essential fatty acids in human skin [2]. They are precursors for synthesis of mediators that are pro-inflammatory or that actively end this process and named for this specific effect, specialized proresolving lipid mediators (SPMs). Upon induction of inflammation resolution, cells that initially triggered inflammation undergo a biochemical paradigm shift, known as “lipid mediator class switch”, during which they stop producing classical proinflammatory mediators and start to actively synthesize SPMs. These include AA-derived lipoxins (LXA4 and LXB4), EPA-derived resolvins and DHA-derived resolvins, protectins and maresins [3].
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