N-acetylcysteine: a promising strategy for alleviating damages induced by maternal deprivation in neonatal rats.

Maternal deprivation in the postnatal period triggers complex conditions along with impairment in brain development. Research indicates that N-acetyl-L-cysteine (NAC), a nootropic agent, restores glutathione levels for antioxidant protection in neurons. It also balances neurotransmitters and alleviates irritability and anxiety symptoms by reducing oxidative damage. Micro-RNA-146a plays a significant role in neuroinflammation in individuals with autism spectrum disorder, and its expression is upregulated in brain regions involved in cognitive function. This study assessed the effects of NAC on autistic-like behaviors and miRNA146a gene expression in an animal model of maternal deprivation. Rats were divided into four groups: control, NAC-treated, maternal deprivation model, and maternal deprivation model treated with NAC. Rats in the maternal deprivation model groups were deprived of their mothers for 10 consecutive days (3 h/day), starting at postnatal day 1 (PND1) or 24 h after birth. From PND30, the treated groups received gastric gavage of NAC at 150 mg/kg body weight for 30 days. Behavioral tests were performed at PND61, and brain tissue samples were collected to assess miRNA146a gene expression levels using real time PCR. This study indicates that NAC treatment alleviated repetitive and anxiety-like behaviors and improved exploration and sociability in the maternal deprivation model group. It also significantly reduced the overexpression of miRNA146a gene. These findings suggest that NAC may be a promising dietary supplement or therapeutic candidate for behavioral disorders caused by maternal deprivation. The protective effect of NAC likely occurred through the downregulation of miRNA146a gene expression.