Brivaracitam Ameliorates Increased Inflammation, Oxidative Stress, and Acetylcholinesterase Activity in Ischemic Mice
Chhaya Deval1, Poonam Sharma1, Bhupesh Sharma2, Bhagwat Singh1
1Department of Pharmacology, Amity Institute of Pharmacy, Amity University Uttar Pradesh, Noida, Uttar Pradesh, India
2Department of Pharmaceutical Sciences, Faculty of Life Sciences, Gurugram University, Gurugram, India
Correspondence to: Bhupesh Sharma
Department of Pharmaceutical Sciences, Faculty of Life Sciences, Gurugram University, Nirvana Rd, Mayfield Garden, Sector 51, Gurugram, Samaspur, Haryana 122003, India
E-mail: drbhupeshresearch@gmail.com
ORCID: https://orcid.org/0000-0002-3423-007X

Poonam Sharma
Department of Pharmacology, Amity Institute of Pharmacy, Amity University Uttar Pradesh, Sector 125, Noida, Uttar Pradesh 201303, India
E-mail: psharmabrain@gmail.com
ORCID: https://orcid.org/0000-0003-1889-3743
Received: July 1, 2024; Revised: October 9, 2024; Accepted: November 9, 2024; Published online: November 26, 2024.
© The Korean College of Neuropsychopharmacology. All rights reserved.

This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
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 protein 2A 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, 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, reduced glutathione, catalase, superoxide dismutase), inflammation (tumor necrosis factor- and interleukin-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.
Keywords: Ischemia; Reperfusion injury; Brivaracetam; Oxidative stress; Inflammation; Infarction

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