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.

Liver X receptors (LXRs) are part of the nuclear receptor superfamily and are cholesteroldetecting receptors. LXRs are commonly found in two isoforms: LXR and LXR. LXRs were initially identified as orphan receptors from a rat cDNA library using an oligonucleotide probe. The regulatory activities of LXR in obesity are the subject of this review. LXRs directly operate on numerous target genes such as ABCA1, ABCG1, ABCG8, GLUT4, and other rate-limiting enzymes such as PEPCK, G6P, and F6P, and so play an important role in the treatment of obesity. LXR may interfere with obesity via several signaling mechanisms. The first is through ABC genes, which promote the clearance of excess bodily cholesterol via the lipid removal route from cholesterol-loaded macrophages and intestinal lumen. The second strategy involves boosting GLUT4 expression by increasing glucose absorption by peripheral tissues, and the third involves inhibiting rate-limiting enzymes PCPCK, G6P, and F6P, which eventually decrease hepatic glucose synthesis. LXR's physiological activities suggest that it might be a promising target for obesity therapy.