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Advanced Neurology
ORIGINAL RESEARCH ARTICLE
Protective effect of pantothenic acid in kainic
acid-induced status eilepticus and associated
neurodegeneration in mice
Souravh Bais*, Renu Kumari Rana, Nirmal Dongre, Gaurav Goyanar,
Aakash Singh Panwar, Alok Kumar Soni, and Shanti Lal Singune
Institute of Pharmaceutical Sciences, Sage University, Indore, India
Abstract
Pantothenic acid (PA) is a water-soluble vitamin (Vitamin B) that has recently been
investigated in various chemical-induced neurotoxicity studies. The present study
was designed to explore the biological importance of PA as a neuromodulator by
releasing monoamine oxidase (MAO)-A and MAO-B in kainic acid (KA)-induced
status epilepticus and the associated neurodegeneration in mice. The mice were
intraperitoneally administered with KA at a dose of 10 mg/kg, and the injection
solution was maintained at pH 7.2 ± 0.1 before the injection. Subsequently, the
mice were observed for various behavioral changes, such as grooming, rearing, hind
limb scratching, urination, defecation, jaw movements, salivation, head nodding,
incidence of convulsions, and their latency or any mortality, which were recorded
during a 4-h period. Further, the animals were euthanized for biochemical and
histopathological analysis. The oxidative stress status was determined by measuring
*Corresponding author: levels of glutathione, superoxide dismutase, nitrites, and catalase enzymes. The
Souravh Bais (Souravh2008.123@ MAO-A and MAO-B activities, which represent an indicator of brain memory function,
rediffmail.com) and the level of tumor necrosis factor alpha, which is an inflammatory marker in brain
Citation: Bais S, Rana RK, tissues, were also measured. The PA pre-treated mice showed a significant increase in
Dongre N, et al., 2022, Protective retention with latency, as demonstrated in the passive avoidance test, which indicate
effect of pantothenic acid in kainic its protective effect against the KA-induced cognitive deficit. The results showed that
acid-induced status eilepticus and
associated neurodegeneration in the anti-oxidative and anti-inflammatory potential of PA is due to the change in lipid
mice. Adv Neuro, 1(2): 40. peroxidation, which may prevent mitochondrial damage in neuronal cell, thereby
https://doi.org/10.36922/an.v1i2.40 conferring neuroprotection.
Received: March 4, 2022
Accepted: July 29, 2022 Keywords: Epilepsy; Kainic acid; Pantothenic acid; Pharmacological activity; Biochemical
Published Online: August 30, 2022 analysis; Histopathology
Copyright: © 2022 Author(s).
This is an Open-Access article
distributed under the terms of the
Creative Commons Attribution 1. Introduction
License, permitting distribution,
and reproduction in any medium, Epilepsy is one of the most prominent neurocognitive conditions . Complex partial
[1]
provided the original work is epilepsy has the poorest prognosis among all patients with temporal lobe epilepsy (TLE),
properly cited.
with 60 – 70% of patients experiencing incurable seizures [1,2] . Furthermore, cognitive
Publisher’s Note: AccScience disorders in human TLE are more frequent but the primary etiology is not clearly known.
[2]
Publishing remains neutral with
regard to jurisdictional claims in Administration of kainic acid (KA) as a single infusion has been reported to cause an
published maps and institutional epileptic state in mice, which results in recurrent seizures and memory impairments [3,4] .
affiliations. KA is a molecular analog of glutamate, an excitatory amino acid neurotransmitter. The
Volume 1 Issue 2 (2022) 1 https://doi.org/10.36922/an.v1i2.40

