(−)-Epicatechin Ameliorates Monosodium Urate-Induced Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and the NF-κB Signaling Pathway
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 a...
| Main Authors: | , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2022-04-01
|
| Series: | Frontiers in Pharmacology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fphar.2022.799552/full |
| _version_ | 1819024985996394496 |
|---|---|
| author | Chenxi Wu Fenfen Li Xiaoxi Zhang Wenjing Xu Yan Wang Yanjing Yao Ziwei Han Daozong Xia |
| author_facet | Chenxi Wu Fenfen Li Xiaoxi Zhang Wenjing Xu Yan Wang Yanjing Yao Ziwei Han Daozong Xia |
| author_sort | Chenxi Wu |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-21T05:03:30Z |
| format | Article |
| id | doaj.art-ca29d8aeaf924b0d9f7eca3a7a73e1ec |
| institution | Directory Open Access Journal |
| issn | 1663-9812 |
| language | English |
| last_indexed | 2024-12-21T05:03:30Z |
| publishDate | 2022-04-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Pharmacology |
| spelling | doaj.art-ca29d8aeaf924b0d9f7eca3a7a73e1ec2022-12-21T19:15:12ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122022-04-011310.3389/fphar.2022.799552799552(−)-Epicatechin Ameliorates Monosodium Urate-Induced Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and the NF-κB Signaling PathwayChenxi Wu0Fenfen Li1Xiaoxi Zhang2Wenjing Xu3Yan Wang4Yanjing Yao5Ziwei Han6Daozong Xia7School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, ChinaAcademy of Chinese Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, ChinaBackground: 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.https://www.frontiersin.org/articles/10.3389/fphar.2022.799552/fullanti-inflammatory(−)-epicatechingouty arthritisNF-κB signaling pathwayNLRP3 inflammasome |
| spellingShingle | Chenxi Wu Fenfen Li Xiaoxi Zhang Wenjing Xu Yan Wang Yanjing Yao Ziwei Han Daozong Xia (−)-Epicatechin Ameliorates Monosodium Urate-Induced Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and the NF-κB Signaling Pathway Frontiers in Pharmacology anti-inflammatory (−)-epicatechin gouty arthritis NF-κB signaling pathway NLRP3 inflammasome |
| title | (−)-Epicatechin Ameliorates Monosodium Urate-Induced Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and the NF-κB Signaling Pathway |
| title_full | (−)-Epicatechin Ameliorates Monosodium Urate-Induced Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and the NF-κB Signaling Pathway |
| title_fullStr | (−)-Epicatechin Ameliorates Monosodium Urate-Induced Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and the NF-κB Signaling Pathway |
| title_full_unstemmed | (−)-Epicatechin Ameliorates Monosodium Urate-Induced Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and the NF-κB Signaling Pathway |
| title_short | (−)-Epicatechin Ameliorates Monosodium Urate-Induced Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and the NF-κB Signaling Pathway |
| title_sort | epicatechin ameliorates monosodium urate induced acute gouty arthritis through inhibiting nlrp3 inflammasome and the nf κb signaling pathway |
| topic | anti-inflammatory (−)-epicatechin gouty arthritis NF-κB signaling pathway NLRP3 inflammasome |
| url | https://www.frontiersin.org/articles/10.3389/fphar.2022.799552/full |
| work_keys_str_mv | AT chenxiwu epicatechinamelioratesmonosodiumurateinducedacutegoutyarthritisthroughinhibitingnlrp3inflammasomeandthenfkbsignalingpathway AT fenfenli epicatechinamelioratesmonosodiumurateinducedacutegoutyarthritisthroughinhibitingnlrp3inflammasomeandthenfkbsignalingpathway AT xiaoxizhang epicatechinamelioratesmonosodiumurateinducedacutegoutyarthritisthroughinhibitingnlrp3inflammasomeandthenfkbsignalingpathway AT wenjingxu epicatechinamelioratesmonosodiumurateinducedacutegoutyarthritisthroughinhibitingnlrp3inflammasomeandthenfkbsignalingpathway AT yanwang epicatechinamelioratesmonosodiumurateinducedacutegoutyarthritisthroughinhibitingnlrp3inflammasomeandthenfkbsignalingpathway AT yanjingyao epicatechinamelioratesmonosodiumurateinducedacutegoutyarthritisthroughinhibitingnlrp3inflammasomeandthenfkbsignalingpathway AT ziweihan epicatechinamelioratesmonosodiumurateinducedacutegoutyarthritisthroughinhibitingnlrp3inflammasomeandthenfkbsignalingpathway AT daozongxia epicatechinamelioratesmonosodiumurateinducedacutegoutyarthritisthroughinhibitingnlrp3inflammasomeandthenfkbsignalingpathway |