Transcription factor Nrf2 suppresses LPS-induced hyperactivation of BV-2 microglial cells.

Koh K; Jang YJ; Yoon K; Cha Y; Lee HJ; Kim J

首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Transcription factor Nrf2 suppresses LPS-induced hyperactivation of BV-2 microglial cells.

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Transcription factor Nrf2 suppresses LPS-induced hyperactivation of BV-2 microglial cells.

机译：转录因子Nrf2抑制LPS诱导的BV-2小胶质细胞的过度活化。

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Microglial hyperactivation is a hallmark of neurodegenerative diseases and the suppression of microglial hyperactivation is being investigated as a means to treat inflammation-mediated neurodegenerative disorders. Here we report that transcription factor Nrf2 in BV-2 microglia, which regulates the expression of phase II antioxidant enzyme genes, decreased the levels of LPS-induced inflammatory cytokines and mediators. These anti-inflammatory effects were not due to Nrf2-mediated up-regulation of phase II enzymes, since over-expression of these enzymes failed to suppress LPS-mediated microglial hyperactivation. However, Nrf2 inhibited LPS-derived increases in p38 MAPK phosphorylation and NF-kappaB activation. This suggests that Nrf2 inhibits microglial hyperactivation by suppressing p38 MAPK and NF-kappaB signaling pathway.

机译：小胶质细胞过度活化是神经退行性疾病的标志，正在研究抑制小胶质细胞过度活化作为治疗炎症介导的神经变性疾病的手段。在这里我们报告，BV-2小胶质细胞中的转录因子Nrf2调节II期抗氧化酶基因的表达，降低了LPS诱导的炎性细胞因子和介质的水平。这些抗炎作用不是由于Nrf2介导的II期酶的上调，因为这些酶的过表达不能抑制LPS介导的小胶质细胞过度活化。但是，Nrf2抑制LPS衍生的p38 MAPK磷酸化和NF-κB激活的增加。这表明Nrf2通过抑制p38 MAPK和NF-κB信号通路抑制小胶质细胞过度活化。

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《Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology》 |2011年第2期|共8页
作者
Koh K; Jang YJ; Yoon K; Cha Y; Lee HJ; Kim J;
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正文语种 eng
中图分类神经病学;
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1. Transcription factor Nrf2 suppresses LPS-induced hyperactivation of BV-2 microglial cells. [J] . Koh K, Jang YJ, Yoon K, Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology . 2011,第1a2期

机译：转录因子Nrf2抑制LPS诱导的BV-2小胶质细胞的过度活化。
2. HNO suppresses LPS-induced inflammation in BV-2 microglial cells via inhibition of NF-kappa B and p38 MAPK pathways [J] . Zhou Yebo, Wu Zhiyuan, Cao Xu, Pharmacological research: The official journal of The Italian Pharmacological Society . 2016,第Null期

机译：HNO通过抑制NF-κB和p38 MAPK途径抑制LPS诱导的BV-2小胶质细胞炎症
3. HNO suppresses LPS-induced inflammation in BV-2 microglial cells via inhibition of NF-kappa B and p38 MAPK pathways [J] . Zhou Yebo, Wu Zhiyuan, Cao Xu, Pharmacological research: The official journal of The Italian Pharmacological Society . 2016,第Null期

机译：通过抑制NF-Kappa B和P38 Mapk途径，HNO在BV-2微胶质细胞中抑制LPS诱导的炎症
4. Quantitative Proteomic Analysis of S-Nitrosylated Proteins in Microglial BV-2 Cells: Antioxidant Effects of the Green Tea Polyphenol (-)-Epigallocatechin-3-Gallate Under Nitrosative Stress [C] . Fanjun Meng, Wenwen Sheng, Justin Purdy, American Society for Mass Spectrometry Conference on Mass Spectrometry and Allied Topics . 2011

机译：微胶质BV-2细胞中S-亚硝基蛋白蛋白的定量蛋白质组学分析：绿茶多酚（ - ） - 氮杂化胁迫下的抗氧化作用 - EpigallocateChin-3-粘滞
5. Molecular mechanisms by which interferon regulatory factor-8 (IRF-8), a member of the IRF family of transcription factors, suppresses tumor progression of both hematopoietic and nonhematopoietic malignancies [D] . Banik, Debarati. 2014

机译：IRF转录因子家族成员干扰素调节因子8（IRF-8）抑制造血和非造血系统恶性肿瘤的分子机制
6. Microglial TonEBP mediates LPS-induced inflammation and memory loss as transcriptional cofactor for NF-κB and AP-1 [O] . Gyu Won Jeong, Hwan Hee Lee, Whaseon Lee-Kwon, 2020

机译：微痛TineBP将LPS诱导的炎症和记忆损失介导作为NF-κB和AP-1的转录辅因子
7. Gua Lou Gui Zhi decoction suppresses LPS-induced activation of the TLR4/NF-κB pathway in BV-2 murine microglial cells [O] . HAIXIA HU, ZUANFANG LI, XIAOQIN ZHU, 2013

机译：Gua Lou Gui Zhi汤剂抑制了BV-2鼠小胶质细胞中的LPS诱导的TLR4 / NF-κB途径激活

Transcription factor Nrf2 suppresses LPS-induced hyperactivation of BV-2 microglial cells.

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