Abstract Title:

Myricetin inhibits NLRP3 inflammasome activation via reduction of ROS-dependent ubiquitination of ASC and promotion of ROS-independent NLRP3 ubiquitination.

Abstract Source:

Toxicol Appl Pharmacol. 2019 Feb 15 ;365:19-29. Epub 2018 Dec 27. PMID: 30594691

Abstract Author(s):

Hanwen Chen, Hui Lin, Shujun Xie, Bo Huang, Yufeng Qian, Kelie Chen, Yuequn Niu, Han-Ming Shen, Jianting Cai, Peiwei Li, Jianhang Leng, Hao Yang, Dajing Xia, Yihua Wu

Article Affiliation:

Hanwen Chen


Myricetin is a plant-derived flavonoid that exhibits diverse pharmacological properties. The NLRP3 (NLR family, pyrin domain-containing 3 protein) inflammasome is a cytosolic multiprotein complex that plays a critical role in the innate immune response and pathogenesis of multiple inflammatory disorders. The present study found that myricetin inhibited NLRP3 inflammasome assembly via promotion of reactive oxygen species (ROS)-independent ubiquitination of NLRP3 and reduction of ROS-dependent ubiquitination of ASC (apoptosis-associated speck-like protein containing a CARD), which disrupted the interaction between ASC and NLRP3 and inhibited ASC oligomerization. This effect was further confirmed in vivo using mouse models of lipopolysaccharide (LPS)-induced sepsis and alum-induced peritonitis. These results suggest the therapeutic value of myricetin by targeting NLRP3-driven inflammatory diseases.

Study Type : In Vitro Study

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