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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-κB
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Glycyrrhizic Acid Promotes M1 Macrophage Polarization in Murine Bone Marrow-Derived Macrophages Associated with the Activation of JNK and NF-κB

机译:甘草酸促进与JNK和NF-κB激活相关的小鼠骨髓来源的巨噬细胞中的M1巨噬细胞极化。

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摘要

The roots and rhizomes ofGlycyrrhizaspecies (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-α, 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 andE. coliK88 by BMDMs and decreased the intracellular survival ofE. coliK88 andS. typhimurium. Moreover, we demonstrated that JNK and NF-κB 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:甘草(甘草)的根和根茎已被广泛用作天然甜味剂和草药。这项研究的目的是研究甘草中的甘草酸(GA)对巨噬细胞极化的影响。 GA评估了小鼠骨髓衍生的巨噬细胞(BMDM)的表型和功能活性。我们的结果表明,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的表达以及TNF-α,IL-12,IL-6和NO(经典激活(M1)巨噬细胞的标志物)的产生,而下调MR,Ym1和Arg1的表达。 (交替激活的(M2)巨噬细胞的标记)。功能测试表明,GA显着提高了FITC-葡聚糖和E的吸收。 BMDMs可导致大肠杆菌K88降低E的细胞内存活率。 coliK88和S。鼠伤寒。此外,我们证明GA诱导NO和M1相关细胞因子的产生需要JNK和NF-κB激活,而ERK1 / 2途径通过诱导IL-10发挥调节作用。总之,这些发现表明GA促进了M1巨噬细胞的极化并增强了其吞噬作用和杀菌能力。结果扩大了我们对GA在巨噬细胞极化中作用的认识。

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