Glycyrrhizin ameliorates experimental colitis through attenuating interleukin-17-producing T cell responses via regulating antigen-presenting cells
Glycyrrhizin ameliorates experimental colitis through attenuating interleukin-17-producing T cell responses via regulating antigen-presenting cells
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甘草酸通过调节抗原呈递细胞来减弱产生白细胞介素 17 的 T 细胞反应,从而改善实验性结肠炎
DOI:
10.1007/s12026-017-8894-2
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发表时间:
2017-06-01
影响因子:
4.4
通讯作者:
Fang, Min
中科院分区:
文献类型:
--
作者:
Chen, Xiangyu;Fang, Dai;Fang, Min
Glycyrrhizin, a component of Chinese medicine licorice root, has the ability to inhibit the functions of high-mobility group box 1 (HMGB1). While glycyrrhizin is known to have anti-inflammatory activities, the underlying mechanisms by which glycyrrhizin inhibits inflammation during the development of trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis are not well understood. This study systemically examined the regulatory effects of glycyrrhizin on inflammatory response in TNBS-induced murine colitis and explored the potential mechanisms involved in this process. We reported that glycyrrhizin treatment ameliorated colitis and decreased the production of inflammatory mediators HMGB1, IFN-γ, IL-6, TNF-α, and IL-17. In addition, glycyrrhizin regulated responses of dendritic cells (DCs) and macrophages during the development of colitis. Furthermore, administration of glycyrrhizin suppressed the proliferation of Th17 cells in colitis. Moreover, the ability of DCs and macrophages to induce the differentiation of Th17 cells was enhanced in presence of HMGB1, which was inhibited by glycyrrhizin. These results demonstrated that glycyrrhizin alleviated colitis by inhibiting the promotive effect of HMGB1 on DC/macrophage-mediated Th17 proliferation. In conclusion, HMGB1 plays an important role in the development of colitis. As an inhibitor of HMGB1, glycyrrhizin might be a novel therapy for colitis.