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二十二碳五烯酸(DPA,22:5n-3)可改善溃疡性结肠炎模型中的炎症。

Docosapentaenoic acid (DPA, 22:5n-3) ameliorates inflammation in an ulcerative colitis model.

机构信息

Institute of Seafood, Zhejiang Gongshang University, Hangzhou 310012, China.

出版信息

Food Funct. 2019 Jul 17;10(7):4199-4209. doi: 10.1039/c8fo02338g.

Abstract

The anti-inflammatory profile of DPA was investigated via a dextran sulphate sodium (DSS)-induced colitis model, and was also compared with those of EPA and DHA. The results showed that DPA could significantly reduce (stronger than EPA and DHA) the disease activity index score, macroscopic appearance score, colon shortening, histological assessment, and myeloperoxidase accumulation in the colon. In addition, DPA also inhibited the abnormal production and mRNA expression of pro-inflammatory cytokines, namely tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 and improved the production and expression of an anti-inflammatory cytokine, IL-10. Furthermore, the molecular mechanisms underlying these effects were also explored through the synthesis pathway of eicosanoids. DPA could inhibit the synthesis of leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) more greatly while differences of cyclooxygenase (COX) and 5-lipoxidase (LOX) contents in these three groups were not significant. We ascribed these effects to the easier incorporation of DPA into inflammatory cells leading to the decrease in the substrate for the synthesis of pro-inflammatory eicosanoids (PGE2 and LTB4). Besides, DPA-derived mediators might also be involved.

摘要

通过葡聚糖硫酸钠(DSS)诱导的结肠炎模型研究了 DPA 的抗炎特性,并将其与 EPA 和 DHA 进行了比较。结果表明,DPA 可显著降低(比 EPA 和 DHA 更强)疾病活动指数评分、宏观外观评分、结肠缩短、组织学评估以及髓过氧化物酶在结肠中的积累。此外,DPA 还抑制了促炎细胞因子(TNF-α、IL-1β 和 IL-6)的异常产生和 mRNA 表达,并改善了抗炎细胞因子 IL-10 的产生和表达。此外,还通过类二十烷酸的合成途径探索了这些作用的分子机制。DPA 可以更强烈地抑制白三烯 B4(LTB4)和前列腺素 E2(PGE2)的合成,而这三组中环氧化酶(COX)和 5-脂氧化酶(LOX)含量的差异不显著。我们将这些作用归因于 DPA 更容易掺入炎症细胞,从而减少了促炎类二十烷酸(PGE2 和 LTB4)合成的底物。此外,DPA 衍生的介质也可能参与其中。

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