Objective: Cerebral ischemia is a medical condition that occurs due to poor supply of blood in the brain. Reperfusion being savage further exaggerates the tissue injury causing cerebral ischemia-reperfusion injury (CI/R). CI/R is marked by an impairment in release of neurotransmitter, excitotoxicity, oxidative stress, inflammation, and neuronal apoptosis. The current study has utilized brivaracetam (BRV), a Synaptic vesicle glycoprotein 2A (SV2A) modulator in experimental model of CI/R injury.
Methods: CI/R injury was induced in Swiss Albino mice by occlusion of common carotid arteries followed by reperfusion. Animals were assessed for learning and memory (MWM), motor coordination (Rota rod, lateral push, and inclined beam walking test), cerebral infarction, and histopathological alterations. Biochemical assessments were made for oxidative stress (thiobarbituric acid reactive species (TBARS), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), inflammation (tumor necrosis factor-TNF-α and interleukin-IL-10), and acetylcholinesterase activity (AChE) in brain supernatants.
Results: CI/R animals showed impairment in learning, memory, and motor coordination, along with increase in cerebral infarction, and histopathological alterations. Furthermore, increase in brain oxidative stress, inflammation, and AChE activity were recorded in CI/R animals. Administration of BRV (10 mg/kg and 20 mg/kg; p.o.) was observed to recuperate CI/R induced impairments in behavioral, biochemical, and histopathological analysis.
Conclusion: It may be concluded that BRV mediates neuroprotection during CI/R via decreasing brain oxidative stress, inflammation, and AChE activity.