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Edaravone Attenuates the Proinflammatory Response in Amyloid-β-Treated Microglia by Inhibiting NLRP3 Inflammasome-Mediated IL-1β Secretion
Author(s) -
Hongmei Wang,
Ting Zhang,
Jiankang Huang,
Jingyan Xiang,
Jingjiong Chen,
Jianliang Fu,
Yuwu Zhao
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000481753
Subject(s) - inflammasome , proinflammatory cytokine , microglia , reactive oxygen species , oxidative stress , mitochondrial ros , chemistry , caspase 1 , superoxide dismutase , microbiology and biotechnology , edaravone , mitochondrion , pharmacology , biochemistry , biology , immunology , inflammation , receptor
Microglial activation is an important pathological feature in the brains of patients with Alzheimer's disease (AD), and amyloid-β (Aβ) peptides play a crucial role in microglial activation. In addition, edaravone (EDA) was recently shown to suppress oxidative stress and proinflammatory cytokine production in APPswePS1dE9 (APP/PS1) mice. However, the mechanism by which EDA inhibits the Aβ-induced proinflammatory response in microglia is poorly understood.

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