Suppr超能文献

海鞘氯仿提取物的抗炎活性。

Anti-inflammatory activity of ethylacetate fraction of Cliona celata.

机构信息

College of Pharmacy, Yeungnam University, Gyeongsan, Republic of Korea.

出版信息

Immunopharmacol Immunotoxicol. 2011 Jun;33(2):373-9. doi: 10.3109/08923973.2010.520716. Epub 2010 Oct 8.

Abstract

We evaluated the ability of the ethylacetate fraction of marine sponge, Cliona celata (ECC), harvested from Korean seaside to regulate the expression of inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)-stimulated murine macrophage-like RAW264.7 cells. ECC dose-dependently inhibited both the expression of iNOS protein and mRNA, resulting in decreased production of nitric oxide (NO), with an IC(50) of 80.5 μg/mL. To investigate action mechanism by which ECC inhibits NO production and iNOS expression, we examined the activation of IκB in LPS-stimulated RAW264.7 cells. ECC clearly inhibited translocation of nuclear factor-κB (NF-κB) p65 subunits from cytosol to nucleus, which correlated with its inhibitory effects on IκB-α phosphorylation and degradation. Furthermore, ECC potently suppressed both the reporter gene expression and DNA-binding activity of NF-κB, which was associated with decreased p65 protein levels in the nucleus. Here, we show for the first time that ECC inhibits NF-κB activation through the inhibition of IκB degradation.

摘要

我们评估了从韩国沿海采集的海洋海绵 Cliona celata(ECC)的乙酸乙酯部分调节脂多糖(LPS)刺激的鼠巨噬细胞样 RAW264.7 细胞中诱导型一氧化氮合酶(iNOS)表达的能力。ECC 呈剂量依赖性抑制 iNOS 蛋白和 mRNA 的表达,导致一氧化氮(NO)的产生减少,IC50 为 80.5 μg/mL。为了研究 ECC 抑制 NO 产生和 iNOS 表达的作用机制,我们检查了 LPS 刺激的 RAW264.7 细胞中 IκB 的激活。ECC 明显抑制核因子-κB(NF-κB)p65 亚基从细胞质向细胞核的易位,这与其对 IκB-α磷酸化和降解的抑制作用相关。此外,ECC 强烈抑制 NF-κB 的报告基因表达和 DNA 结合活性,这与核内 p65 蛋白水平降低有关。在这里,我们首次表明 ECC 通过抑制 IκB 降解来抑制 NF-κB 激活。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验