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Wei Wei
Researcher at Second Military Medical University
Publications - 5
Citations - 268
Wei Wei is an academic researcher from Second Military Medical University. The author has contributed to research in topics: Receptor & Autophagy. The author has an hindex of 5, co-authored 5 publications receiving 206 citations.
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Journal ArticleDOI
Activating cannabinoid receptor 2 alleviates pathogenesis of experimental autoimmune encephalomyelitis via activation of autophagy and inhibiting NLRP3 inflammasome.
TL;DR: Whether autophagy is involved in the beneficial effect of CB2R on EAE is examined and the mechanism with a focus on inflammasome activation is explored.
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Activation of Cannabinoid Receptor 2 Ameliorates DSS-Induced Colitis through Inhibiting NLRP3 Inflammasome in Macrophages
TL;DR: It is concluded that activation of CB2R ameliorates DSS-induced colitis through enhancing autophagy that may inhibit NLRP3 inflammasome activation in macrophages and it is demonstrated that AMPK-mTOR-P70S6K signaling pathway was involved in thisCB2R-mediated process.
Journal ArticleDOI
Autophagy Plays an Important Role in Anti-inflammatory Mechanisms Stimulated by Alpha7 Nicotinic Acetylcholine Receptor.
Bo-Zong Shao,Ping Ke,Zhe-Qi Xu,Wei Wei,Ming-He Cheng,Bin-Ze Han,Xiongwen Chen,Ding-Feng Su,Chong Liu +8 more
TL;DR: It is demonstrated for the first time that activating α7nAChR enhances monocyte/microglia autophagy, which suppresses neuroinflammation and thus plays an alleviative role in EAE.
Journal ArticleDOI
Activating α7 nicotinic acetylcholine receptor inhibits NLRP3 inflammasome through regulation of β-arrestin-1.
TL;DR: To evaluate whether activating α7 nicotinic acetylcholine receptor (α7nAChR) could inhibit the NOD‐like receptor family, pyrin domain containing 3 (NLRP3) inflammasome through regulation of β‐arrestin‐1 in monocyte/macrophage system, thus contributing to the control of neuroinflammation.
Journal ArticleDOI
The protective action of ketanserin against lipopolysaccharide-induced shock in mice is mediated by inhibiting inducible NO synthase expression via the MEK/ERK pathway.
Chong Liu,Xin Zhang,Jv-Xiang Zhou,Wei Wei,Dian-Hua Liu,Ping Ke,Gufang Zhang,Guo-Jun Cai,Ding-Feng Su +8 more
TL;DR: The findings indicate that inhibition of the expression of iNOS via the MEK/ERK pathway mediates the protective effects of ketanserin against LPS-induced shock in mice.