Protective effect of pantothenic acid in kainic acid-induced status eilepticus and associated neurodegeneration in mice

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 levels of glutathione, superoxide dismutase, nitrites, and catalase enzymes. The MAO-A and MAO-B activities, which represent an indicator of brain memory function, and the level of tumor necrosis factor alpha, which is an inflammatory marker in brain tissues, were also measured. The PA pre-treated mice showed a significant increase in retention with latency, as demonstrated in the passive avoidance test, which indicate its protective effect against the KA-induced cognitive deficit. The results showed that the anti-oxidative and anti-inflammatory potential of PA is due to the change in lipid peroxidation, which may prevent mitochondrial damage in neuronal cell, thereby conferring neuroprotection.