首页> 外文期刊>Mediators of inflammation >Glycyrrhizic Acid Promotes M1 Macrophage Polarization in Murine Bone Marrow-Derived Macrophages Associated with the Activation of JNK and NF-kappa B
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Glycyrrhizic Acid Promotes M1 Macrophage Polarization in Murine Bone Marrow-Derived Macrophages Associated with the Activation of JNK and NF-kappa B

机译:甘草酸促进鼠骨髓源自巨噬细胞的M1巨噬细胞极化与JNK和NF-Kappa B的激活相关的巨噬细胞

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摘要

The roots and rhizomes of Glycyrrhiza species (licorice) have been widely used as natural sweeteners and herbal medicines. The aim of this study is to investigate the effect of glycyrrhizic acid (GA) from licorice on macrophage polarization. Both phenotypic and functional activities of murine bone marrow-derived macrophages (BMDMs) treated by GA were assessed. Our results showed that GA obviously increased the cell surface expression of CD80, CD86, and MHCII molecules. Meanwhile, GA upregulated the expression of CCR7 and the production of TNF-alpha, IL-12, IL-6, and NO (the markers of classically activated (M1) macrophages), whereas it downregulated the expression of MR, Ym1, and Arg1 (the markers of alternatively activated (M2) macrophage). The functional tests showed that GA dramatically enhanced the uptake of FITC-dextran and E. coli K88 by BMDMs and decreased the intracellular survival of E. coli K88 and S. typhimurium. Moreover, we demonstrated that JNK and NF-kappa B activation are required for GA-induced NO and M1-related cytokines production, while ERK1/2 pathway exhibits a regulatory effect via induction of IL-10. Together, these findings indicated that GA promoted polarization of M1 macrophages and enhanced its phagocytosis and bactericidal capacity. The results expanded our knowledge about the role of GA in macrophage polarization.
机译:Glycyrrhiza物种(甘草)的根和根茎已被广泛用作天然甜味剂和草药。本研究的目的是探讨甘草酸(GA)对甘草极化甘草酸(GA)的影响。评估GA处理的鼠骨髓衍生的巨噬细胞(BMDMS)的表型和功能活性。我们的研究结果表明,GA明显增加了CD80,CD86和MHCII分子的细胞表面表达。同时,GA上调CCR7的表达和TNF-α,IL-12,IL-6的产生(典型活化(M1)巨噬细胞的标志物),而它下调了MR,YM1和ARG1的表达(可选地激活(M2)巨噬细胞的标记)。功能试验表明,GA显着增强了BMDMS的FITC-DEXTRAN和大肠杆菌K88的摄取,并降低了大肠杆菌K88和伤寒伤寒的细胞内存活。此外,我们证明了GA诱导的NO和M1相关细胞因子产生所需的JNK和NF-Kappa B活化,而ERK1 / 2途径通过诱导IL-10表现出调节效果。这些研究结果在一起表明,GA促进了M1巨噬细胞的极化,增强了吞噬作用和杀菌能力。结果扩展了我们对Ga在巨噬细胞极化中的作用的了解。

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  • 来源
    《Mediators of inflammation》 |2015年第8期|共12页
  • 作者单位

    Zhejiang Univ Coll Anim Sci Educ Minist Key Lab Anim Mol Nutr Hangzhou 310058 Zhejiang;

    Zhejiang Univ Coll Anim Sci Educ Minist Key Lab Anim Mol Nutr Hangzhou 310058 Zhejiang;

    Zhejiang Univ Coll Anim Sci Educ Minist Key Lab Anim Mol Nutr Hangzhou 310058 Zhejiang;

    Zhejiang Univ Coll Anim Sci Educ Minist Key Lab Anim Mol Nutr Hangzhou 310058 Zhejiang;

    Zhejiang Univ Coll Anim Sci Educ Minist Key Lab Anim Mol Nutr Hangzhou 310058 Zhejiang;

    Zhejiang Univ Coll Anim Sci Educ Minist Key Lab Anim Mol Nutr Hangzhou 310058 Zhejiang;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 病理学;
  • 关键词

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