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

• Main Authors: Chenxi Wu (Author), Fenfen Li (Author), Xiaoxi Zhang (Author), Wenjing Xu (Author), Yan Wang (Author), Yanjing Yao (Author), Ziwei Han (Author), Daozong Xia (Author)
• Format: Book
• Published: Frontiers Media S.A., 2022-04-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

Background: 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.Methods and results: 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 in vitro. 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 in vitro and in vivo.Conclusion: These results indicated that EC could effectively improve MSU-induced acute gouty arthritis via inhibiting NLRP3 inflammasome and the NF-κB signaling pathway in vitro and in vivo, which suggested that EC might be a promising active ingredient for the prevention and treatment of gouty arthritis.

Item Description

1663-9812
10.3389/fphar.2022.799552