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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
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