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

J Neuroimmunol. 2011 Apr;233(1-2):160-7. doi: 10.1016/j.jneuroim.2011.01.004. Epub 2011 Feb 23.

Abstract

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-κB activation. This suggests that Nrf2 inhibits microglial hyperactivation by suppressing p38 MAPK and NF-κB signaling pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Cytokines / metabolism
  • Gene Expression Regulation, Enzymologic / physiology
  • Gliosis / genetics
  • Gliosis / immunology*
  • Gliosis / metabolism
  • Lipopolysaccharides / antagonists & inhibitors*
  • Lipopolysaccharides / pharmacology*
  • Mice
  • Microglia / enzymology
  • Microglia / immunology*
  • Microglia / metabolism*
  • NF-E2-Related Factor 2 / genetics*
  • NF-kappa B / metabolism
  • Signal Transduction / genetics
  • Signal Transduction / immunology
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Cytokines
  • Lipopolysaccharides
  • NF-E2-Related Factor 2
  • NF-kappa B
  • Nfe2l2 protein, mouse
  • p38 Mitogen-Activated Protein Kinases