Protective Effects of Catechin against Monosodium Urate-Induced Inflammation through the Modulation of NLRP3 Inflammasome Activation

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• 作者：Jhih-Jia Jhang ; Chi-Cheng Lu ; Cheng-Ying Ho ; Yu-Ting Cheng ; Gow-Chin Yen
• 刊名：Journal of Agricultural and Food Chemistry
• 出版年：2015
• 出版时间：August 26, 2015
• 年：2015
• 卷：63
• 期：33
• 页码：7343-7352
• 全文大小：491K
• ISSN：1520-5118

文摘

Gouty inflammation results from the stimulation of monosodium urate (MSU). Interleukin-1尾 (IL-1尾) secretion is the primary clinical manifestation of MSU attack, and MSU activates IL-1尾 through a nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome. This study investigated the protective effect and underlying mechanism of naturally occurring phenolic compounds on MSU-induced inflammation in vivo and in vitro. A screening of phenolic compounds revealed that gallic acid and catechin exhibited the most potent free radical scavenging activities. Subcutaneous injection of gallic acid or catechin significantly reduced MSU-induced IL-1尾 and IL-6 secretion in C57BL/6 mice. However, only catechin inhibited MSU-induced IL-1尾 secretion and NLRP3 inflammasome activation in MSU-challenged THP-1 cells. MSU-triggered mitochondrial reactive oxygen species (MtROS) production and intracellular calcium levels were significantly decreased by treatment with catechin in THP-1 cells. Catechin treatment also up-regulated Bcl-2 levels and restored MSU-induced mitochondrial transmembrane potential impairment. These results indicate that the protective effects of catechin on MSU-induced IL-1尾 secretion are associated with modulation of mitochondrial damage. It also suggests that catechin has the potential to protect gout attack by modulation of NLRP3 inflammasome activation.