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(-)-表儿茶素通过抑制NLRP3炎性小体和NF-κB信号通路改善尿酸钠诱导的急性痛风性关节炎

(-)-Epicatechin Ameliorates Monosodium Urate-Induced Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and the NF-κB Signaling Pathway.

作者信息

Wu Chenxi, Li Fenfen, Zhang Xiaoxi, Xu Wenjing, Wang Yan, Yao Yanjing, Han Ziwei, Xia Daozong

机构信息

School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.

Academy of Chinese Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.

出版信息

Front Pharmacol. 2022 Apr 6;13:799552. doi: 10.3389/fphar.2022.799552. eCollection 2022.

DOI:10.3389/fphar.2022.799552
PMID:35462936
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9019746/
Abstract

Gouty arthritis is a common and complex inflammatory disease that will reduce the life quality of human beings (-)-Epicatechin (EC) is famous for antioxidant and anti-inflammatory activities. Thus, the aim of this study was to investigate the therapeutic effect of EC on gouty arthritis and its mechanisms. EC was added into a monosodium urate (MSU)-stimulated THP-1 cell that was induced by phorbol 12-myristate 13-acetate and lipopolysaccharide (LPS) in advance to establish a gout model . The efficiency of EC on acute gouty arthritis mice induced by MSU was further investigated. The results showed that EC concentration-dependently improved the cell viability of LPS and MSU stimulated THP-1 cells, and significantly alleviated MSU-induced ankle edema in mice in a dose-dependent manner. In addition, EC inhibited the infiltration of inflammatory cells and local cascular congestion in ankle joint tissue. Furthermore, the secretion of inflammatory cytokines (IL-1β, IL-18, IL-6, and TNF-α) activation of NLRP3 inflammasome and NF-κB signaling pathway were markedly suppressed by EC and . These results indicated that EC could effectively improve MSU-induced acute gouty arthritis via inhibiting NLRP3 inflammasome and the NF-κB signaling pathway and , which suggested that EC might be a promising active ingredient for the prevention and treatment of gouty arthritis.

摘要

痛风性关节炎是一种常见且复杂的炎症性疾病,会降低人类的生活质量。(-)-表儿茶素(EC)以其抗氧化和抗炎活性而闻名。因此,本研究的目的是探讨EC对痛风性关节炎的治疗作用及其机制。预先将EC添加到由佛波醇12-肉豆蔻酸酯13-乙酸酯和脂多糖(LPS)诱导的尿酸钠(MSU)刺激的THP-1细胞中,以建立痛风模型。进一步研究了EC对MSU诱导的急性痛风性关节炎小鼠的疗效。结果表明,EC浓度依赖性地提高了LPS和MSU刺激的THP-1细胞的细胞活力,并以剂量依赖性方式显著减轻了MSU诱导的小鼠踝关节水肿。此外,EC抑制了踝关节组织中炎症细胞的浸润和局部血管充血。此外,EC显著抑制了炎症细胞因子(IL-1β、IL-18、IL-6和TNF-α)的分泌以及NLRP3炎性小体和NF-κB信号通路的激活。这些结果表明,EC可通过抑制NLRP3炎性小体和NF-κB信号通路有效改善MSU诱导的急性痛风性关节炎,这表明EC可能是预防和治疗痛风性关节炎的一种有前景的活性成分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/2e99b57d93ce/fphar-13-799552-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/e25f355ee065/fphar-13-799552-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/279be75d00da/fphar-13-799552-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/e6e62c5ab9e7/fphar-13-799552-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/20b009bc1d18/fphar-13-799552-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/d85001c65ffd/fphar-13-799552-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/2e99b57d93ce/fphar-13-799552-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/e25f355ee065/fphar-13-799552-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/5a0fb8a1eea2/fphar-13-799552-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/279be75d00da/fphar-13-799552-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/d5af5555a1f4/fphar-13-799552-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/e6e62c5ab9e7/fphar-13-799552-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/20b009bc1d18/fphar-13-799552-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/d85001c65ffd/fphar-13-799552-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/9019746/2e99b57d93ce/fphar-13-799552-g008.jpg

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