• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
Nrf2 activator Diethyl Maleate attenuates ROS mediated NLRP3 inflammasome activation in murine microglia.Nrf2激活剂马来酸二乙酯减轻活性氧介导的小鼠小胶质细胞中NLRP3炎性小体激活。
Cytotechnology. 2024 Apr;76(2):197-208. doi: 10.1007/s10616-023-00609-8. Epub 2023 Nov 28.
2
Melatonin Attenuates LPS-Induced Acute Depressive-Like Behaviors and Microglial NLRP3 Inflammasome Activation Through the SIRT1/Nrf2 Pathway.褪黑素通过 SIRT1/Nrf2 通路减轻 LPS 诱导的急性抑郁样行为和小胶质细胞 NLRP3 炎性小体激活。
Front Immunol. 2019 Jul 2;10:1511. doi: 10.3389/fimmu.2019.01511. eCollection 2019.
3
Dimethyl Fumarate Alleviates NLRP3 Inflammasome Activation in Microglia and Sickness Behavior in LPS-Challenged Mice.富马酸二甲酯可减轻脂多糖刺激的小胶质细胞中 NLRP3 炎性小体的激活和小鼠的病态行为。
Front Immunol. 2021 Nov 10;12:737065. doi: 10.3389/fimmu.2021.737065. eCollection 2021.
4
Sulforaphane inhibits NLRP3 inflammasome activation in microglia through Nrf2-mediated miRNA alteration.萝卜硫素通过Nrf2介导的miRNA改变抑制小胶质细胞中NLRP3炎性小体的激活。
Immunol Lett. 2021 May;233:20-30. doi: 10.1016/j.imlet.2021.03.004. Epub 2021 Mar 9.
5
β-adrenoceptor agonist formoterol attenuates NLRP3 inflammasome activation and GSDMD-mediated pyroptosis in microglia through enhancing IκBα/NF-κB inhibition, SQSTM1/p62-dependent selective autophagy and ESCRT-III-mediated plasma membrane repair.β-肾上腺素受体激动剂福莫特罗通过增强 IκBα/NF-κB 抑制、SQSTM1/p62 依赖性选择性自噬和 ESCRT-III 介导的质膜修复,减弱小胶质细胞中的 NLRP3 炎性体激活和 GSDMD 介导热激。
Mol Cell Neurosci. 2024 Sep;130:103956. doi: 10.1016/j.mcn.2024.103956. Epub 2024 Aug 2.
6
Targeting NLRP3 Inflammasome With Nrf2 Inducers in Central Nervous System Disorders.靶向 NLRP3 炎性小体与中枢神经系统疾病中的 Nrf2 诱导剂。
Front Immunol. 2022 Mar 28;13:865772. doi: 10.3389/fimmu.2022.865772. eCollection 2022.
7
Tenuigenin protects dopaminergic neurons from inflammation via suppressing NLRP3 inflammasome activation in microglia.金雀异黄素通过抑制小胶质细胞中 NLRP3 炎性体的激活来保护多巴胺能神经元免受炎症损伤。
J Neuroinflammation. 2017 Dec 20;14(1):256. doi: 10.1186/s12974-017-1036-x.
8
3-(Naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride attenuates NLRP3 inflammasome-mediated signaling pathway in lipopolysaccharide-stimulated BV2 microglial cells.盐酸3-(萘-2-基(丙氧基)甲基)氮杂环丁烷可减弱脂多糖刺激的BV2小胶质细胞中NLRP3炎性小体介导的信号通路。
Biochem Biophys Res Commun. 2018 Jan 1;495(1):151-156. doi: 10.1016/j.bbrc.2017.10.131. Epub 2017 Oct 27.
9
CB2R activation ameliorates late adolescent chronic alcohol exposure-induced anxiety-like behaviors during withdrawal by preventing morphological changes and suppressing NLRP3 inflammasome activation in prefrontal cortex microglia in mice.CB2R 激活通过防止形态变化和抑制前额叶皮层小胶质细胞中 NLRP3 炎性体激活,改善了青少年晚期慢性酒精暴露戒断期间的焦虑样行为。
Brain Behav Immun. 2023 May;110:60-79. doi: 10.1016/j.bbi.2023.02.001. Epub 2023 Feb 6.
10
Anthocyanins from L. Inhibit NLRP3 Inflammasome in BV2 Microglia Cells by Alleviating NF-B- and ER Stress-Induced Ca Accumulation and Mitochondrial ROS Production.蓝莓花色苷通过减轻 NF-κB 和内质网应激诱导的 Ca2+ 积累和线粒体 ROS 产生来抑制 BV2 小胶质细胞中的 NLRP3 炎性体。
Oxid Med Cell Longev. 2021 Feb 4;2021:1246491. doi: 10.1155/2021/1246491. eCollection 2021.

引用本文的文献

1
Mechanism and role of H. pylori CagA-induced NLRP3 inflammasome in gastric cancer immune cell infiltration.幽门螺杆菌CagA诱导的NLRP3炎性小体在胃癌免疫细胞浸润中的机制及作用
Sci Rep. 2025 Apr 24;15(1):14335. doi: 10.1038/s41598-025-98301-8.

本文引用的文献

1
Potential Therapeutic Use of the Rosemary Diterpene Carnosic Acid for Alzheimer's Disease, Parkinson's Disease, and Long-COVID through NRF2 Activation to Counteract the NLRP3 Inflammasome.迷迭香二萜类化合物鼠尾草酸通过激活NRF2对抗NLRP3炎性小体在阿尔茨海默病、帕金森病和长期新冠中的潜在治疗用途
Antioxidants (Basel). 2022 Jan 6;11(1):124. doi: 10.3390/antiox11010124.
2
Nrf2/Keap1/ARE signaling: Towards specific regulation.Nrf2/Keap1/ARE 信号通路:走向特异性调控。
Life Sci. 2022 Feb 15;291:120111. doi: 10.1016/j.lfs.2021.120111. Epub 2021 Oct 31.
3
The Nrf2-NLRP3-caspase-1 axis mediates the neuroprotective effects of Celastrol in Parkinson's disease.姜黄素通过 Nrf2-NLRP3-caspase-1 轴对帕金森病发挥神经保护作用。
Redox Biol. 2021 Nov;47:102134. doi: 10.1016/j.redox.2021.102134. Epub 2021 Sep 22.
4
FOXO transcription factors in antioxidant defense.FOXO 转录因子在抗氧化防御中的作用。
IUBMB Life. 2022 Jan;74(1):53-61. doi: 10.1002/iub.2542. Epub 2021 Aug 23.
5
Neurodegenerative Disease and the NLRP3 Inflammasome.神经退行性疾病与NLRP3炎性小体
Front Pharmacol. 2021 Mar 10;12:643254. doi: 10.3389/fphar.2021.643254. eCollection 2021.
6
Sulforaphane inhibits NLRP3 inflammasome activation in microglia through Nrf2-mediated miRNA alteration.萝卜硫素通过Nrf2介导的miRNA改变抑制小胶质细胞中NLRP3炎性小体的激活。
Immunol Lett. 2021 May;233:20-30. doi: 10.1016/j.imlet.2021.03.004. Epub 2021 Mar 9.
7
The KEAP1-NRF2 System as a Molecular Target of Cancer Treatment.KEAP1-NRF2系统作为癌症治疗的分子靶点
Cancers (Basel). 2020 Dec 26;13(1):46. doi: 10.3390/cancers13010046.
8
NRF2 and the Ambiguous Consequences of Its Activation during Initiation and the Subsequent Stages of Tumourigenesis.NRF2及其在肿瘤发生起始阶段和后续阶段激活所产生的不确定后果
Cancers (Basel). 2020 Dec 2;12(12):3609. doi: 10.3390/cancers12123609.
9
Targeting the microglial NLRP3 inflammasome and its role in Parkinson's disease.靶向小胶质细胞 NLRP3 炎性体及其在帕金森病中的作用。
Mov Disord. 2020 Jan;35(1):20-33. doi: 10.1002/mds.27874. Epub 2019 Nov 4.
10
Microglia Biology: One Century of Evolving Concepts.小胶质细胞生物学:百年演变概念。
Cell. 2019 Oct 3;179(2):292-311. doi: 10.1016/j.cell.2019.08.053.

Nrf2激活剂马来酸二乙酯减轻活性氧介导的小鼠小胶质细胞中NLRP3炎性小体激活。

Nrf2 activator Diethyl Maleate attenuates ROS mediated NLRP3 inflammasome activation in murine microglia.

作者信息

Kiser Cagla, Gonul Ceren Perihan, Genc Sermin

机构信息

Izmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Mithatpasa St. 58/5 Balcova, 35340 Izmir, Turkey.

Izmir International Biomedicine and Genome Institute, Dokuz Eylul University, Izmir, Turkey.

出版信息

Cytotechnology. 2024 Apr;76(2):197-208. doi: 10.1007/s10616-023-00609-8. Epub 2023 Nov 28.

DOI:10.1007/s10616-023-00609-8
PMID:38495294
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10940551/
Abstract

Microglia are the tissue-resident immune cells of the central nervous system. As a part of the innate immune response, NLR Family Pyrin Domain Containing Protein 3 (NLRP3) inflammasome activation leads to cleavage of caspase-1 and triggers secretion of proinflammatory cytokines and may also result in pyroptotic cell death. Inflammasome activation plays a crucial role in inflammatory conditions; aberrant activation of inflammasome contributes to the pathogenesis of neurodegenerative diseases. Diethyl Maleate (DEM) is a promising antiinflammatory chemical to alleviate inflammasome activation. In this study, NLRP3 inflammasome was activated in N9 murine microglia via 1 µg/ml LPS (Lipopolysaccharide) for 4 h and 5 mM ATP (Adenosine 5'-triphosphate) for 1 h, respectively. We demonstrated that 1 h pretreatment of DEM attenuated NLRP3 inflammasome activation in microglial cells. Besides, mitochondrial ROS decreased upon DEM pretreatment in inflammasome-induced cells. Likewise, it ameliorated pyroptotic cell death in microglia. DEM is a potent activator of Nrf2 transcription factor, the key regulator of the antioxidant response pathway. Nrf2 has been a significant target to decrease aberrant inflammasome activation through the antioxidant compounds, including DEM. Here, we have shown that DEM increased Nrf2 translocation to the nucleus, resulting in Nrf2 target gene expression in microglia. In conclusion, DEM is a promising protective agent against NLRP3 inflammasome activation.

摘要

小胶质细胞是中枢神经系统中的组织驻留免疫细胞。作为固有免疫反应的一部分,含NLR家族pyrin结构域蛋白3(NLRP3)炎性小体的激活会导致半胱天冬酶-1的裂解,并触发促炎细胞因子的分泌,还可能导致细胞焦亡。炎性小体的激活在炎症状态中起关键作用;炎性小体的异常激活会导致神经退行性疾病的发病机制。马来酸二乙酯(DEM)是一种有前景的抗炎化学物质,可减轻炎性小体的激活。在本研究中,分别通过1μg/ml脂多糖(LPS)处理4小时和5mM三磷酸腺苷(ATP)处理1小时,在N9小鼠小胶质细胞中激活NLRP3炎性小体。我们证明,DEM预处理1小时可减弱小胶质细胞中NLRP3炎性小体的激活。此外,在炎性小体诱导的细胞中,DEM预处理后线粒体活性氧减少。同样,它改善了小胶质细胞中的细胞焦亡。DEM是Nrf2转录因子的有效激活剂,Nrf2是抗氧化反应途径的关键调节因子。Nrf2一直是通过包括DEM在内的抗氧化化合物减少异常炎性小体激活的重要靶点。在这里,我们表明DEM增加了Nrf2向细胞核的转位,导致小胶质细胞中Nrf2靶基因的表达。总之,DEM是一种有前景的针对NLRP3炎性小体激活的保护剂。