Selective COX-2 Inhibitors as Neuroprotective Agents in Traumatic Brain Injury.
Matthew I HiskensAnthony G SchneidersAndrew S FenningPublished in: Biomedicines (2024)
Traumatic brain injury (TBI) is a significant contributor to mortality and morbidity in people, both young and old. There are currently no approved therapeutic interventions for TBI. Following TBI, cyclooxygenase (COX) enzymes generate prostaglandins and reactive oxygen species that perpetuate inflammation, with COX-1 and COX-2 isoforms providing differing responses. Selective COX-2 inhibitors have shown potential as neuroprotective agents. Results from animal models of TBI suggest potential treatment through the alleviation of secondary injury mechanisms involving neuroinflammation and neuronal cell death. Additionally, early clinical trials have shown that the use of celecoxib improves patient mortality and outcomes. This review aims to summarize the therapeutic effects of COX-2 inhibitors observed in TBI animal models, highlighting pertinent studies elucidating molecular pathways and expounding upon their mechanistic actions. We then investigated the current state of evidence for the utilization of COX-2 inhibitors for TBI patients.
Keyphrases
- traumatic brain injury
- severe traumatic brain injury
- cell death
- clinical trial
- end stage renal disease
- reactive oxygen species
- cerebral ischemia
- chronic kidney disease
- oxidative stress
- ejection fraction
- newly diagnosed
- cardiovascular events
- metabolic syndrome
- cardiovascular disease
- type diabetes
- physical activity
- cell proliferation
- prognostic factors
- case report
- mass spectrometry
- coronary artery disease
- human health
- peritoneal dialysis
- mild traumatic brain injury
- randomized controlled trial
- brain injury
- climate change
- middle aged
- cognitive impairment
- combination therapy