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Resolvin D5, a Lipid Mediator, Inhibits Production of Interleukin-6 and CCL5 Via the ERK-NF-κB Signaling Pathway in Lipopolysaccharide-Stimulated THP-1 Cells.
Journal of Microbiology and Biotechnology ( IF 2.5 ) Pub Date : 2019-11-7 , DOI: 10.4014/jmb.1907.07033
Hyun-Woo Chun 1 , Jintak Lee 1 , Thu-Huyen Pham 1 , Jiyon Lee 1 , Jae-Hwan Yoon 1 , Jin Lee 1 , Deok-Kun Oh 1 , Jaewook Oh 2 , Do-Young Yoon 1
Affiliation  

One of the omega-3 essential fatty acids, docosahexaenoic acid (DHA), is a significant constituent of the cell membrane and the precursor of several potent lipid mediators. These mediators are considered to be important in preventing or treating several diseases. Resolvin D5, an oxidized lipid mediator derived from DHA, has been known to exert anti-inflammatory effects. However, the detailed mechanism underlying these effects has not yet been elucidated in human monocytic THP-1 cells. In the present study, we investigated the effects of resolvin D5 on inflammation-related signaling pathways, including the extracellular signal-regulated kinase (ERK)-nuclear factor (NF)-κB signaling pathway. Resolvin D5 downregulated the production of interleukin (IL)-6 and chemokine (C-C motif) ligand 5 (CCL5). Additionally, these inhibitory effects were found to be modulated by mitogen-activated protein kinase (MAPK) and NF-κB in lipopolysaccharide (LPS)-treated THP-1 cells. Resolvin D5 inhibited the LPS-stimulated phosphorylation of ERK and translocation of p65 and p50 into the nucleus, resulting in the inhibition of IL-6 and CCL5 production. These results revealed that resolvin D5 exerts anti-inflammatory effects in LPS-treated THP-1 cells by regulating the phosphorylation of ERK and nuclear translocation of NF-kappaB.

中文翻译:

Resolvin D5 是一种脂质介质,可在脂多糖刺激的 THP-1 细胞中通过 ERK-NF-κB 信号通路抑制 Interleukin-6 和 CCL5 的产生。

omega-3 必需脂肪酸之一,二十二碳六烯酸 (DHA),是细胞膜的重要成分,也是几种有效脂质介质的前体。这些介质被认为对预防或治疗多种疾病很重要。已知 Resolvin D5 是一种源自 DHA 的氧化脂质介质,具有抗炎作用。然而,这些影响的详细机制尚未在人单核细胞 THP-1 细胞中阐明。在本研究中,我们研究了 resolvin D5 对炎症相关信号通路的影响,包括细胞外信号调节激酶 (ERK)-核因子 (NF)-κB 信号通路。Resolvin D5 下调白细胞介素 (IL)-6 和趋化因子(CC 基序)配体 5 (CCL5) 的产生。此外,这些抑制作用被发现受脂多糖 (LPS) 处理的 THP-1 细胞中丝裂原活化蛋白激酶 (MAPK) 和 NF-κB 的调节。Resolvin D5 抑制 LPS 刺激的 ERK 磷酸化以及 p65 和 p50 易位到细胞核中,从而抑制 IL-6 和 CCL5 的产生。这些结果表明,resolvin D5 通过调节 ERK 的磷酸化和 NF-kappaB 的核转位,在 LPS 处理的 THP-1 细胞中发挥抗炎作用。
更新日期:2020-08-21
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