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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Resolvin E1, an endogenous lipid mediator derived from omega-3 eicosapentaenoic acid, protects against 2,4,6-trinitrobenzene sulfonic acid-induced colitis
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Resolvin E1, an endogenous lipid mediator derived from omega-3 eicosapentaenoic acid, protects against 2,4,6-trinitrobenzene sulfonic acid-induced colitis

机译：Resolvin E1是源自omega-3二十碳五烯酸的内源性脂质介体，可抵抗2,4,6-三硝基苯磺酸引起的结肠炎

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摘要

Resolvin E1 (RvE1; 55,12R,18R-trihydroxyeicosapentaenoic acid) is an antiinflammatory lipid mediator derived from omega-3 fatty acid eicosapentaenoic acid (EPA). At the local site of inflammation, aspirin treatment enhances EPA conversion to 18R-oxygenated products, including RvE1, which carry potent antiinflammatory signals. Here, we obtained evidence for reduced leukocyte infiltration in a mouse peritonitis model, where the administration of EPA and aspirin initiated the generation of RvE1 in the exudates. Similar results were obtained with the administration of synthetic RvE1, which blocked leukocyte infiltration. RvE1 also protected against the development of 2,4,6-trinitrobenzene sulfonic acid-induced colitis. The beneficial effect was reflected by increased survival rates, sustained body weight, improvement of histologic scores, reduced serum anti-2,4,6-trinitrobenzene sulfonic acid lgG, decreased leukocyte infiltration, and proinflammatory gene expression, including IL-12 p40, TNF-α, and inducible nitric oxide synthase. Thus, the endogenous lipid mediator RvE1 counter-regulates leukocyte-mediated tissue injury and proinflammatory gene expression. These findings show an endogenous mechanism that may underlie the beneficial actions of omega-3 EPA and provide targeted approaches for the treatment of intestinal inflammation.
机译：Resolvin E1（RvE1; 55,12R，18R-三羟基二十碳五烯酸）是一种抗炎脂质介体，衍生自omega-3脂肪酸二十碳五烯酸（EPA）。在炎症的局部部位，阿司匹林治疗可增强EPA转化为18R氧化产物（包括RvE1）的能力，这些产物携带有效的抗炎信号。在这里，我们获得了在小鼠腹膜炎模型中白细胞浸润减少的证据，在该模型中，EPA和阿司匹林的施用引发了渗出液中RvE1的产生。合成RvE1的使用获得了类似的结果，它阻断了白细胞的浸润。 RvE1还可以防止2,4,6-三硝基苯磺酸诱导的结肠炎的发展。存活率提高，体重持续增加，组织学评分提高，血清抗2,4,6-三硝基苯磺酸lgG降低，白细胞浸润减少以及促炎性基因表达（包括IL-12 p40，TNF）反映出了有益的作用。 -α和诱导型一氧化氮合酶。因此，内源性脂质介体RvE1反调节白细胞介导的组织损伤和促炎基因表达。这些发现表明，内源性机制可能是omega-3 EPA有益作用的基础，并提供了治疗肠道炎症的靶向方法。

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