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Chrysanthemum indicum extract inhibits NLRP3 and AIM2 inflammasome activation via regulating ASC phosphorylation

Chrysanthemum indicum (C. indicum), a perennial plant, has long been used to treat inflammation-related disorders, such as pneumonia, hypertension, gastritis, and gastroenteritis. The inhibitory effect of C. indicum extract (C.I) on inflammasome activation was investigated to validate its potential...

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Bibliographic Details
Published in:Journal of ethnopharmacology 2019-07, Vol.239, p.111917-111917, Article 111917
Main Authors: Yu, Sang-Hyeun, Sun, Xiao, Kim, Myong-Ki, Akther, Mahbuba, Han, Jun-Hyuk, Kim, Tae-Yeon, Jiang, Jun, Kang, Tae-Bong, Lee, Kwang-Ho
Format: Article
Language:English
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Summary:Chrysanthemum indicum (C. indicum), a perennial plant, has long been used to treat inflammation-related disorders, such as pneumonia, hypertension, gastritis, and gastroenteritis. The inhibitory effect of C. indicum extract (C.I) on inflammasome activation was investigated to validate its potential in treating inflammation related disorders. LPS-primed bone marrow-derived macrophages (BMDMs) were used to confirm the inhibitory effect of C.I on selective inflammasome activation in vitro. A monosodium urate (MSU)-induced murine peritonitis model was employed to study the effect of C.I in vivo. C.I inhibited activation of NLRP3 and AIM2 inflammasomes, leading to suppression of interleukin-1β secretion in vitro. Further, C.I regulates the phosphorylation of apoptosis-associated speck-like protein containing a CARD (ASC), which could be the main contribution to attenuate these inflammasomes activation. C.I also suppressed secretion of pro-inflammatory cytokines and neutrophils recruitment in MSU-induced murine peritonitis model. This study provides scientific evidence substantiating the traditional use of C. indicum in the treatment of inflammatory diseases, including gout, which is induced by physiologically analogous cause to MSU-induced peritonitis. [Display omitted]
ISSN:0378-8741
1872-7573
DOI:10.1016/j.jep.2019.111917