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NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
Published on: January 12, 2020
Transcription factor Nrf2 suppresses LPS-induced hyperactivation of BV-2 microglial cells
Kyungmi Koh1, Jaekyoon Kim, Young Jin Jang
1School of Biological Sciences, Seoul National University, Seoul 151-921, Republic of Korea.
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.
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