期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 233, 期 1-2, 页码 160-167出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2011.01.004
关键词
Nrf2; Microglia; p38; NF-kappa B; NQO1; Glutathione
资金
- Korea Research Foundation [KRF-2008-313-C00757]
- Brain Research Center of the 21st Century Frontier Research Program [2010 K000829]
- World Class University Program [R31-2008-00-10056-0]
- National Research Foundation
- Ministry of Education, Science and Technology, Republic of Korea
- National Research Foundation of Korea [2008-313-C00757] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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-kappa B activation. This suggests that Nrf2 inhibits microglial hyperactivation by suppressing p38 MAPK and NF-kappa B signaling pathway. (C) 2011 Elsevier B.V. All rights reserved.
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