Abstract
Autism spectrum disorder, or individual disability (ID), is a condition characterized by complications in social interaction, restricted repetitive behavior, and difficulties in social communication. Neuquinon (NQ) possess a powerful therapeutic potential in various neurodegenerative disease. Nevertheless, contributing to NQ's low water solubility and bioavailability, its medicinal use has been constrained. Liposomes were supposed to be prospective drug-delivering agents for NQ, crossing the blood-brain barrier (BBB), and reaching the target organs. The current investigation aims to track the signaling pathways that govern NQ and liposomal neuquinon (LNQ) action in autistic models generated by ethyl formic acid. The neurotransmitters gamma amino-butyric acid (GABA), acetylcholine (ACh), and acetylcholinesterase (AChE) in addition to, the gene expressions of brain-derived neurotrophic factor (BDNF), cAMP response element-binding protein (CREB), and methyl-CpG-binding protein 2 (MeCP2) and the DNA damage COMET analysis at different time intervals of the study, were assessed. EFA in a dose of 500 mg/kg BW was used to induce autism in rats, and then NQ and LNQ were administered in 10 mg/kg and 2 mg/kg BW, respectively. The results revealed that NQ and LNQ significantly down-regulated BDNF, GABA, and AChE; on the other hand, they up-regulated MeCP2, CREB gene expressions, and ACh action. NQ and LNQ displayed improvement in DNA damage in almost all brain regions after EFA alterations; even better results were noticed post-LNQ therapy. Therefore, it may be concluded that neuquinon and liposomal-loaded neuquinon have a therapeutic index versus EFA-induced autism in a rat model.