This study investigates the role of NADPH oxidase 2 (NOX2) in the development of brain edema and cognitive impairment following traumatic brain injury (TBI). The researchers explored how NOX2 influences the expression of aquaporin-4 (AQP4), a water channel protein implicated in cerebral edema, and assessed the effects of NOX2 inhibition on cognitive outcomes post-TBI.
Genetic deletion of NOX2 resulted in decreased AQP4 expression and reduced edema in the hippocampus and cortex following TBI. Inhibiting AQP4 pharmacologically or through genetic deletion attenuated neurological deficits without altering reactive oxygen species levels. These findings suggest that NOX2 contributes to cognitive impairment post-TBI by modulating AQP4-mediated brain edema.
The study utilized NOX2 Knockout (NOX2−/−) mice to assess the impact of NOX2 deletion on AQP4 expression, brain edema, and cognitive functions after TBI.
Traumatic brain injury, Cognitive impairment, Brain edema, NADPH oxidase 2, Aquaporin-4
Gene Knockout, Traumatic brain injury model, Cognitive function assessment, Western blotting, Brain water content measurement
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