Epigallocatechin gallate inhibits urate crystals-induced peritoneal inflammation in C57BL/6 mice

被引:63
作者
Jhang, Jhih-Jia [1 ]
Lu, Chi-Cheng [1 ]
Yen, Gow-Chin [1 ]
机构
[1] Natl Chung Hsing Univ, Dept Food Sci & Biotechnol, Taichung, Taiwan
关键词
EGCG; IL-1; beta; Inflammation; MSU; NLRP3; GREEN TEA; NALP3; INFLAMMASOME; OXIDATIVE STRESS; GOUT; ACTIVATION; MACROPHAGES; (-)-EPIGALLOCATECHIN-3-GALLATE; MECHANISMS; IL-1-BETA; SECRETION;
D O I
10.1002/mnfr.201600106
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Gouty arthritis is a type of monosodium urate (MSU) crystals-induced inflammation in the articular tissue and shows the increased levels of neutrophil infiltration and IL-1 beta secretion. MSU is capable of activating IL-1 beta through a nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome. Epigallocatechin gallate (EGCG), a bioactive polyphenol in green tea with potent antioxidant activity, is effective to prevent rheumatoid arthritis and osteoarthritis. However, it remains unclear whether EGCG improves gouty inflammation. This study aimed to investigate the effect of EGCG on MSU-induced inflammation and NLRP3 inflammasome activation. C57BL/6 mice were received subcutaneous injection or oral gavage of EGCG before the intraperitoneal injection of MSU. The results demonstrated that EGCG inhibited MSU-induced neutrophil infiltration and IL1 beta secretion. Furthermore, EGCG decreased MSU-triggered neutrophil cytosolic factor 1 and NLRP3 protein expression, limiting pro-inflammatory mediator secretion such as IL-1 beta, IL6, monocyte chemoattractant protein-1, and serum amyloid A. In addition, EGCG treatment suppressed NLRP3 inflammasome activation in MSU-challenged THP-1 monocytes. These findings indicate that EGCG treatment ameliorates MSU-induced inflammation, suggesting that EGCG exerts anti-inflammatory effect against MSU-induced acute gout attack.
引用
收藏
页码:2297 / 2303
页数:7
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