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本文引用的文献

1
Critical role of NLRP3-caspase-1 pathway in age-dependent isoflurane-induced microglial inflammatory response and cognitive impairment.NLRP3-caspase-1 通路在年龄相关的异氟醚诱导小胶质细胞炎症反应和认知功能障碍中的关键作用。
J Neuroinflammation. 2018 Apr 17;15(1):109. doi: 10.1186/s12974-018-1137-1.
2
NLRP3-dependent synaptic plasticity deficit in an Alzheimer's disease amyloidosis model in vivo.体内阿尔茨海默病淀粉样变性模型中 NLRP3 依赖性突触可塑性缺陷。
Neurobiol Dis. 2018 Jun;114:24-30. doi: 10.1016/j.nbd.2018.02.016. Epub 2018 Feb 23.
3
The NLRP3 inflammasome: Role in metabolic disorders and regulation by metabolic pathways.NLRP3 炎性体：在代谢紊乱中的作用及其代谢途径的调节。
Cancer Lett. 2018 Apr 10;419:8-19. doi: 10.1016/j.canlet.2018.01.034. Epub 2018 Jan 12.
4
Specific inhibition of NLRP3 in chikungunya disease reveals a role for inflammasomes in alphavirus-induced inflammation.特异性抑制寨卡病毒病中的 NLRP3 炎症小体揭示了炎症小体在甲病毒诱导的炎症中的作用。
Nat Microbiol. 2017 Oct;2(10):1435-1445. doi: 10.1038/s41564-017-0015-4. Epub 2017 Aug 28.
5
Purinergic 2X7 receptor/NLRP3 pathway triggers neuronal apoptosis after ischemic stroke in the mouse.嘌呤能 2X7 受体/NLRP3 途径在小鼠缺血性卒中后引发神经元凋亡。
Exp Neurol. 2017 Jun;292:46-55. doi: 10.1016/j.expneurol.2017.03.002. Epub 2017 Mar 6.
6
Inhibiting the NLRP3 inflammasome with MCC950 promotes non-phlogistic clearance of amyloid-β and cognitive function in APP/PS1 mice.MCC950 抑制 NLRP3 炎性小体可促进 APP/PS1 小鼠淀粉样-β的非炎症性清除和认知功能改善。
Brain Behav Immun. 2017 Mar;61:306-316. doi: 10.1016/j.bbi.2016.12.014. Epub 2016 Dec 18.
7
Novel extracellular and nuclear caspase-1 and inflammasomes propagate inflammation and regulate gene expression: a comprehensive database mining study.新型细胞外和细胞核中的半胱天冬酶-1及炎性小体介导炎症并调控基因表达：一项全面的数据库挖掘研究
J Hematol Oncol. 2016 Nov 14;9(1):122. doi: 10.1186/s13045-016-0351-5.
8
Inflammasome Complexes: Emerging Mechanisms and Effector Functions.炎性小体复合物：新出现的机制与效应功能
Cell. 2016 May 5;165(4):792-800. doi: 10.1016/j.cell.2016.03.046.
9
Inhibition of Alveolar Macrophage Pyroptosis Reduces Lipopolysaccharide-induced Acute Lung Injury in Mice.抑制肺泡巨噬细胞焦亡可减轻脂多糖诱导的小鼠急性肺损伤
Chin Med J (Engl). 2015 Oct 5;128(19):2638-45. doi: 10.4103/0366-6999.166039.
10
A Mitochondrion-Targeted Antioxidant Ameliorates Isoflurane-Induced Cognitive Deficits in Aging Mice.一种线粒体靶向抗氧化剂可改善异氟烷诱导的衰老小鼠认知缺陷。
PLoS One. 2015 Sep 17;10(9):e0138256. doi: 10.1371/journal.pone.0138256. eCollection 2015.

NLRP3 炎性小体依赖性细胞焦亡被认为参与了年龄相关的异氟醚诱导认知障碍的机制。

NLRP3 inflammasome-dependent pyroptosis is proposed to be involved in the mechanism of age-dependent isoflurane-induced cognitive impairment.

机构信息

Department of Anesthesiology, Shanghai Pudong New Area People's Hospital, Shanghai, 201200, China.

Wannan Medical College, Anhui, 241003, China.

出版信息

J Neuroinflammation. 2018 Sep 14;15(1):266. doi: 10.1186/s12974-018-1299-x.

DOI:10.1186/s12974-018-1299-x
PMID:30217191
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6138927/
Abstract

Wang Z et al. recently published a paper, titled "Critical role of NLRP3-caspase-1 pathway in age-dependent isoflurane-induced microglial inflammatory response and cognitive impairment". The finding in this paper is consistent with our previous study on NLRP3-caspase-1 pathway. Here, we propose that NLRP3 inflammasome-dependent pyroptosis may be involved in the mechanism of age-dependent isoflurane-induced cognitive impairment and discuss that inhibiting NLRP3 inflammasome activation with a novel inhibitor MCC950 may ameliorate age-dependent isoflurane-induced neuro-inflammation.

摘要

王志等人最近发表了一篇题为“NLRP3-caspase-1 通路在年龄依赖性异氟醚诱导的小胶质细胞炎症反应和认知障碍中的关键作用”的论文。该研究结果与我们之前关于 NLRP3-caspase-1 通路的研究一致。在这里，我们提出 NLRP3 炎性体依赖性细胞焦亡可能参与年龄依赖性异氟醚诱导的认知障碍的机制，并讨论了用新型抑制剂 MCC950 抑制 NLRP3 炎性体的激活可能改善年龄依赖性异氟醚诱导的神经炎症。