首页> 美国卫生研究院文献>other >Lysophosphatidylcholine Triggers TLR2- and TLR4-Mediated Signaling Pathways but Counteracts LPS-Induced NO Synthesis in Peritoneal Macrophages by Inhibiting NF-κB Translocation and MAPK/ERK Phosphorylation

【2h】

Lysophosphatidylcholine Triggers TLR2- and TLR4-Mediated Signaling Pathways but Counteracts LPS-Induced NO Synthesis in Peritoneal Macrophages by Inhibiting NF-κB Translocation and MAPK/ERK Phosphorylation

机译：溶血磷脂酰胆碱触发TLR2和TLR4介导的信号通路但通过抑制NF-κB易位和MAPK / ERK磷酸化来抵消LPS诱导的腹膜巨噬细胞中NO的合成。

代理获取

本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。

页面导航

摘要
著录项
相似文献
相关主题

摘要

BackgroundLysophosphatidylcholine (LPC) is the main phospholipid component of oxidized low-density lipoprotein (oxLDL) and is usually noted as a marker of several human diseases, such as atherosclerosis, cancer and diabetes. Some studies suggest that oxLDL modulates Toll-like receptor (TLR) signaling. However, effector molecules that are present in oxLDL particles and can trigger TLR signaling are not yet clear. LPC was previously described as an attenuator of sepsis and as an immune suppressor. In the present study, we have evaluated the role of LPC as a dual modulator of the TLR-mediated signaling pathway.

机译：背景溶血磷脂酰胆碱（LPC）是氧化的低密度脂蛋白（oxLDL）的主要磷脂成分，通常被认为是多种人类疾病的标志物，例如动脉粥样硬化，癌症和糖尿病。一些研究表明oxLDL调节Toll样受体（TLR）信号传导。但是，尚不清楚oxLDL粒子中存在的并能触发TLR信号传导的效应分子。 LPC以前被描述为败血症的减毒剂和免疫抑制剂。在本研究中，我们评估了LPC作为TLR介导的信号通路的双重调节剂的作用。

著录项

期刊名称 other
作者
Alan Brito Carneiro; Bruna Maria Ferreira Iaciura; Lilian Lie Nohara; Carla Duque Lopes; Esteban Mauricio Cordero Veas; Vania Sammartino Mariano; Patricia Torres Bozza; Ulisses Gazos Lopes; Georgia Correa Atella; Igor Correia Almeida; Mário Alberto Cardoso Silva-Neto;
展开▼
作者单位

展开▼
年(卷),期 -1(8),9
年度 -1
页码 e76233
总页数 9
原文格式 PDF
正文语种
中图分类
关键词

相似文献

外文文献
中文文献
专利

1. Ugonin M, a Helminthostachys zeylanica Constituent, Prevents LPS-Induced Acute Lung Injury through TLR4-Mediated MAPK and NF-κB Signaling Pathways [J] . Kun-Chang Wu, Shyh-Shyun Huang, Yueh-Hsiung Kuo, Molecules . 2017,第4期

机译：Ugonin M是一种Helminthostachys zeylanica成分，可通过TLR4介导的MAPK和NF-κB信号传导途径预防LPS诱导的急性肺损伤
2. Ugonin M, a Helminthostachys zeylanica Constituent, Prevents LPS-Induced Acute Lung Injury through TLR4-Mediated MAPK and NF-κB Signaling Pathways [J] . Kun-Chang Wu, Shyh-Shyun Huang, Yueh-Hsiung Kuo, Molecules . 2017,第4期

机译：Ugonin M是一种Helminthostachys zeylanica成分，可通过TLR4介导的MAPK和NF-κB信号传导途径预防LPS诱导的急性肺损伤
3. Epigallocatechin-3-gallate Inhibits LPS-Induced NF-κB and MAPK Signaling Pathways in Bone Marrow-Derived Macrophages [J] . So-Young Joo, Young-A Song, Young-Lan Park, Gut and Liver . 2012,第2期

机译：Epigallocatechin-3-gallate抑制LPS诱导的骨髓巨噬细胞中的NF-κB和MAPK信号通路
4. Ugonin M a Helminthostachys zeylanica Constituent Prevents LPS-Induced Acute Lung Injury through TLR4-Mediated MAPK and NF-κB Signaling Pathways [O] . Kun-Chang Wu, Shyh-Shyun Huang, Yueh-Hsiung Kuo, 2017

机译：Ugonin M是一种Helminthostachys zeylanica成分可通过TLR4介导的MAPK和NF-κB信号传导途径防止LPS诱导的急性肺损伤
5. Lysophosphatidylcholine triggers TLR2- and TLR4-mediated signaling pathways but counteracts LPS-induced NO synthesis in peritoneal macrophages by inhibiting NF-κB translocation and MAPK/ERK phosphorylation. [O] . Alan Brito Carneiro, Bruna Maria Ferreira Iaciura, Lilian Lie Nohara, 2013

机译：溶血磷脂酰胆碱触发TLR2和TLR4介导的信号传导途径，但通过抑制NF-κB易位和mapK / ERK磷酸化来抵消腹膜巨噬细胞中Lps诱导的NO合成。

Lysophosphatidylcholine Triggers TLR2- and TLR4-Mediated Signaling Pathways but Counteracts LPS-Induced NO Synthesis in Peritoneal Macrophages by Inhibiting NF-κB Translocation and MAPK/ERK Phosphorylation

摘要

著录项

相似文献

相关主题

期刊订阅