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Activating alpha 7 nicotinic acetylcholine receptor inhibits NLRP3 inflammasome through regulation of beta-arrestin-1

文献类型： 外文期刊

作者： Ke, Ping 1 ; Shao, Bo-Zong 1 ; Xu, Zhe-Qi 1 ; Chen, Xiong-Wen 3 ; Wei, Wei 4 ; Liu, Chong 1 ;

作者机构： 1.Second Mil Med Univ, Dept Pharmacol, Shanghai, Peoples R China

2.Nanjing Mil Command, Naval Convalescent Zone Hangzhou Sanat, Nanjing, Jiangsu, Peoples R China

3.Temple Univ, Sch Med, Cardiovasc Res Ctr, Philadelphia, PA 19122 USA

4.Zhejiang Acad Agr Sci, Inst Qual & Standard Agroprod, State Key Lab Breeding Base Zhejiang Sustainable, Zhejiang Prov Key Lab Food Safety, Hangzhou, Zhejiang, Peoples R China

关键词： alpha 7nAChR;beta-arrestin-1;neuroinflammation;NLRP3 inflammasome

期刊名称：CNS NEUROSCIENCE & THERAPEUTICS （ 影响因子：5.243； 五年影响因子：4.977 ）

ISSN： 1755-5930

年卷期： 2017 年 23 卷 11 期

页码：

收录情况： SCI

摘要： AimsTo evaluate whether activating 7 nicotinic acetylcholine receptor (7nAChR) could inhibit the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome through regulation of -arrestin-1 in monocyte/macrophage system, thus contributing to the control of neuroinflammation. MethodsThe protein levels of NLRP3, caspase-1 (Casp-1) p20 and proCasp-1, interleukin-1 (IL-1) p17 and proIL-1, IL-18 and proIL-18 were measured using Western blotting. The mRNA levels of Casp-1 and IL-1 were detected by real-time PCR (RT-PCR). The colocalization and interaction of NLRP3 protein and -arrestin-1 were measured by immunofluorescence staining and immunoprecipitation. ResultsThe expression of -arrestin-1 was significantly increased and colocalized with CD45-positive cells in spinal cord of experimental auto-immune encephalomyelitis (EAE) mice when compared with the sham mice, which was attenuated by pretreatment with PNU282987, a specific 7nAChR agonist. PNU282987 also significantly inhibited the activation of NLRP3 inflammasome and thus decreased the production of IL-1 and IL-18 both in lipopolysaccharide (LPS)/ATP-stimulated BV2 microglia in vitro and spinal cord from EAE mice in vivo, while inverse effects were observed in 7nAChR knockout mice. Furthermore, overexpression of -arrestin-1 attenuated the inhibitory effect of PNU282987 on NLRP3 inflammasome activation in LPS/ATP-stimulated BV2 microglia. PNU282987 inhibited the interaction between -arrestin-1 and NLRP3 protein in vitro. ConclusionsThe present study demonstrates that activating 7nAChR can lead to NLRP3 inflammasome inhibition via regulation of -arrestin-1 in monocyte/microglia system.

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[1]Activating Cannabinoid Receptor 2 Alleviates Pathogenesis of Experimental Autoimmune Encephalomyelitis Via Activation of Autophagy and Inhibiting NLRP3 Inflammasome. Shao, Bo-Zong,Ke, Ping,Xu, Zhe-Qi,Zhou, Jv-Xiang,Liu, Chong,Wei, Wei. 2014

[2]Autophagy Plays an Important Role in Anti-inflammatory Mechanisms Stimulated by Alpha7 Nicotinic Acetylcholine Receptor. Shao, Bo-Zong,Ke, Ping,Xu, Zhe-Qi,Cheng, Ming-He,Han, Bin-Ze,Su, Ding-Feng,Liu, Chong,Wei, Wei,Chen, Xiong-Wen. 2017

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