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大黄酸在体内和体外通过抑制核因子κB和NLRP3炎性小体减轻炎症。

Rhein attenuates inflammation through inhibition of NF-κB and NALP3 inflammasome in vivo and in vitro.

作者信息

Ge Hui, Tang Hao, Liang Yanbing, Wu Jingguo, Yang Qing, Zeng Lijin, Ma Zhongfu

机构信息

Department of Health Care Clinic, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

Department of General Internal Medicine, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

出版信息

Drug Des Devel Ther. 2017 Jun 6;11:1663-1671. doi: 10.2147/DDDT.S133069. eCollection 2017.

DOI:10.2147/DDDT.S133069
PMID:28652704
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5472410/
Abstract

Rhein is an important component in traditional Chinese herbal medicine formulations for gastrointestinal disorders, including inflammatory bowel diseases such as ulcerative colitis. In this study, we investigated the beneficial effects of rhein in inflammation models in the transgenic zebrafish line TG (corolla eGFP), in which both macrophages and neutrophils express eGFP and RAW264.7 macrophages. We found that the tail-cutting-induced migration of immune cells was significantly reduced in transgenic zebrafish treated with rhein. In addition, the production of proinflammatory cytokines, including IL-6, IL-1β, and tumor necrosis factor-α, were significantly reduced in lipopolysaccharide (LPS)-induced RAW264.7 macrophages treated with rhein. Parallel to the inhibition of proinflammatory cytokines, rhein significantly reduced phosphorylation levels of NF-κB p65 and inducible nitric oxide synthase, as well as COX-2 protein expression levels. Furthermore, rhein significantly reduced NALP3 and cleaved IL-1β expression in LPS + ATP-induced RAW264.7 macrophages. Thus, the present study demonstrates that rhein may exhibit its anti-inflammatory action via inhibition of NF-κB and NALP3 inflammasome pathways.

摘要

大黄素是用于治疗胃肠道疾病(包括溃疡性结肠炎等炎症性肠病)的传统中药配方中的一种重要成分。在本研究中,我们研究了大黄素在转基因斑马鱼品系TG(花冠eGFP)炎症模型中的有益作用,在该模型中巨噬细胞和中性粒细胞均表达eGFP以及RAW264.7巨噬细胞。我们发现,用大黄素处理的转基因斑马鱼中,剪尾诱导的免疫细胞迁移显著减少。此外,在用大黄素处理的脂多糖(LPS)诱导的RAW264.7巨噬细胞中,包括IL-6、IL-1β和肿瘤坏死因子-α在内的促炎细胞因子的产生显著减少。与促炎细胞因子的抑制作用平行,大黄素显著降低了NF-κB p65和诱导型一氧化氮合酶的磷酸化水平,以及COX-2蛋白表达水平。此外,大黄素显著降低了LPS + ATP诱导的RAW264.7巨噬细胞中NALP3和裂解的IL-1β表达。因此,本研究表明大黄素可能通过抑制NF-κB和NALP3炎性小体途径发挥其抗炎作用。

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