The NOX2-ROS-NLRP3 inflammasome axis in traumatic brain injury.

ABSTRACT:

Background

Phagocyte NADPH oxidase 2 (NOX2) is an enzyme complex responsible for reactive oxygen species (ROS) production. Chronic NOX2 activity sustains oxidative stress/damage and drives neuroinflammation following traumatic brain injury (TBI). NOX2 acts as a priming signal for NLRP3 inflammasome activation, which also plays a role in secondary injury after TBI. GSK2795039 is a small molecule brain penetrable drug that inhibits NOX2 in a NADPH competitive manner. Here, we investigated whether pharmacological inhibition of NOX2 using GSK2795039 can reduce secondary neuroinflammation after TBI, specifically via inhibition of downstream NLRP3 inflammasome activation, in both resident microglia and infiltrating myeloid cells in the injured brain.

Methods

Immortalised microglia

SUBMITTER: Laabei J 

PROVIDER: S-EPMC12560392 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature