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

Cagla Kiser1,2, Ceren Perihan Gonul1,2, Sermin Genc1,3

  • 1Izmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Mithatpasa St. 58/5 Balcova, 35340 Izmir, Turkey.

Cytotechnology
|March 18, 2024
PubMed

Insights

Diethyl Maleate (DEM) effectively reduces NLRP3 inflammasome activation in microglia by decreasing mitochondrial ROS and pyroptosis. This protective effect is mediated by DEM-induced Nrf2 activation, highlighting its therapeutic potential for neuroinflammation.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Microglia are key immune cells in the central nervous system.
  • NLRP3 inflammasome activation drives neuroinflammation and neurodegenerative diseases.
  • Diethyl Maleate (DEM) shows potential anti-inflammatory properties.

Purpose of the Study:

  • To investigate DEM's effect on NLRP3 inflammasome activation in microglia.
  • To explore DEM's impact on mitochondrial ROS and pyroptosis.
  • To determine DEM's role in Nrf2 pathway activation.

Main Methods:

  • Activated NLRP3 inflammasome in N9 murine microglia using LPS and ATP.
  • Pretreated microglia with DEM before inflammasome activation.
  • Assessed NLRP3 inflammasome activation, mitochondrial ROS levels, pyroptosis, and Nrf2 translocation.

Main Results:

  • DEM pretreatment significantly attenuated NLRP3 inflammasome activation.
  • DEM reduced mitochondrial ROS and pyroptotic cell death in microglia.
  • DEM enhanced Nrf2 translocation to the nucleus and Nrf2 target gene expression.

Conclusions:

  • DEM effectively inhibits NLRP3 inflammasome activation in microglia.
  • DEM exerts protective effects by reducing oxidative stress and pyroptosis via Nrf2 activation.
  • DEM is a promising therapeutic agent for neuroinflammatory conditions.