| Literature DB >> 33424855 |
Chun-Hsien Wu1,2, Chin Heng Gan3, Lan-Hui Li4,5, Jen-Che Chang6, Shin-Tai Chen6, Mridula P Menon6, Shu-Meng Cheng1, Shih-Ping Yang1, Chen-Lung Ho7, Oleg V Chernikov8, Chi-Hung Lin2,9, Yulin Lam3, Kuo-Feng Hua5,6,10.
Abstract
Conjugated polyenes are a class of widely occurring natural products with various biological functions. We previously identified 4-hydroxy auxarconjugatin B (4-HAB) as anti-inflammatory agent with an IC50 of ~20 µM. In this study, we synthesized a new anti-inflammatory 4-HAB analogue, F240B, which has an IC50 of less than 1 µM. F240B dose-dependently induced autophagy by increasing autophagic flux, LC3 speck formation and acidic vesicular organelle formation. F240B inhibited NACHT, LRR and PYD domain-containing protein 3 (NLRP3) inflammasome activation through autophagy induction. In a mechanistic study, F240B inhibited interleukin (IL)-1β (IL-1β) precursor expression, promoted degradation of NLRP3 and IL-1β, and reduced mitochondrial membrane integrity loss in an autophagy-dependent manner. Additionally, F240B inhibited apoptosis-associated speck-like protein containing a CARD (ASC) oligomerization and speck formation without affecting the interaction between NLRP3 and ASC or NIMA-related kinase 7 (NEK7) and double-stranded RNA-dependent kinase (PKR). Furthermore, F240B exerted in vivo anti-inflammatory activity by reducing the intraperitoneal influx of neutrophils and the levels of IL-1β, active caspase-1, IL-6 and monocyte chemoattractant protein-1 (MCP-1) in lavage fluids in a mouse model of uric acid crystal-induced peritonitis. In conclusion, F240B attenuated the NLRP3 inflammasome through autophagy induction and can be developed as an anti-inflammatory agent in the future.Entities:
Keywords: NLRP3 inflammasome; autophagy; conjugated polyenes; mitochondria; peritonitis
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Year: 2020 PMID: 33424855 PMCID: PMC7793731 DOI: 10.3389/fimmu.2020.607564
Source DB: PubMed Journal: Front Immunol ISSN: 1664-3224 Impact factor: 7.561