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(9Z,11E)-13-氧代十八碳-9,11-二烯酸(13-KODE)源自罗伊氏乳杆菌,通过抑制NF-κB和MAPK以及激活Nrf2/HO-1信号通路对脂多糖刺激的小鼠巨噬细胞产生抗炎作用。

Anti-Inflammatory Effects of (9Z,11E)-13-Oxooctadeca-9,11-dienoic Acid (13-KODE) Derived from L. on Lipopolysaccharide-Stimulated Murine Macrophage via NF-kB and MAPK Inhibition and Nrf2/HO-1 Signaling Activation.

作者信息

Ko Yu-Chan, Choi Hack Sun, Kim Su-Lim, Yun Bong-Sik, Lee Dong-Sun

机构信息

Interdisciplinary Graduate Program in Advanced Convergence Technology & Science, Jeju National University, Jeju 63243, Korea.

Subtropical/Tropical Organism Gene Bank, Jeju National University, Jeju 63243, Korea.

出版信息

Antioxidants (Basel). 2022 Jan 18;11(2):180. doi: 10.3390/antiox11020180.

Abstract

Glasswort ( L.) is a halophyte that exhibits antioxidant and antidiabetic effects. Only a few studies have been conducted on its antioxidant effects. Here, we isolated an antioxidant using an activity-based purification method, and the resulting compound was identified as (9Z,11E)-13-Oxooctadeca-9,11-dienoic acid (13-KODE). We investigated its ability to suppress inflammatory responses and the molecular mechanisms underlying these abilities using lipopolysaccharide-stimulated RAW 264.7 macrophage cells. We studied the anti-inflammatory effects of 13-KODE derived from L on RAW 264.7 macrophages. 13-KODE inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) production by suppressing inducible NO synthase and suppressed LPS-induced tumor necrosis factor and interleukin-1β expression in RAW 264.7 macrophages. LPS-mediated nuclear localization of NF-κB and mitogen-activated protein kinase activation were inhibited by 13-KODE. 13-KODE significantly reduced LPS-induced production of reactive oxygen species and increased the expression of nuclear factor erythroid-2 like 2 (Nfe2I2) and heme oxygenase 1. Overall, our results indicate that 13-KODE may have potential for treating inflammation.

摘要

盐角草(L.)是一种具有抗氧化和抗糖尿病作用的盐生植物。关于其抗氧化作用的研究较少。在此,我们采用基于活性的纯化方法分离出一种抗氧化剂,鉴定该化合物为(9Z,11E)-13-氧代十八碳-9,11-二烯酸(13-KODE)。我们使用脂多糖刺激的RAW 264.7巨噬细胞研究了其抑制炎症反应的能力以及这些能力背后的分子机制。我们研究了源自盐角草的13-KODE对RAW 264.7巨噬细胞的抗炎作用。13-KODE通过抑制诱导型一氧化氮合酶来抑制脂多糖(LPS)诱导的一氧化氮(NO)生成,并抑制RAW 264.7巨噬细胞中LPS诱导的肿瘤坏死因子和白细胞介素-1β表达。13-KODE抑制了LPS介导的核因子κB的核定位和丝裂原活化蛋白激酶的激活。13-KODE显著降低了LPS诱导的活性氧生成,并增加了核因子红细胞2样2(Nfe2I2)和血红素加氧酶1的表达。总体而言,我们的结果表明13-KODE可能具有治疗炎症的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5dd/8868157/f252ae46ee1e/antioxidants-11-00180-g001.jpg

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