Ethanol (EtOH) has been linked to neurotoxic effects on the fetus and prenatal alcohol exposure (PAE) has a negative impact on brain neurodevelopment. Therefore, the present study was aimed to focus on the underlying mechanisms of alcohol-induced oxidative stress and apoptotic cell death in addition to shedding the light on the modulatory effect of nanocurcumin in rats’ offspring prefrontal cortices. The current study investigated the effects of prenatal maternal exposure to EtOH intragastric (i.g.) administration of 0.015 mL/g of a 10 % v/v ethanol solution throughout gestation and the concomitant use of nanocurcumin, on 21-day-old offspring Wistar rat prefrontal cortex parameters. CYP2E1, DBN1, DNMT1, miRNA-335, miRNA-21, c-Fos and Cox-2 gene expression as well as the accompanying histological and ultrastructural alterations were assessed. The implemented experimental setting has revealed that ethanol exposure caused significant alterations in the above mentioned parameters. Changes observed in nanocurcumin-treated animals were significantly different to the ethanol-treated group when nanocurcumin was concomitantly administered.

乙醇 (EtOH) 与对胎儿的神经毒性作用有关，产前酒精暴露 (PAE) 对大脑神经发育有负面影响。因此，本研究的目的是除了阐明纳米姜黄素对大鼠后代前额叶皮质的调节作用外，还重点研究酒精诱导的氧化应激和细胞凋亡的潜在机制。目前的研究调查了产前母亲在整个妊娠期间暴露于 EtOH 胃内 (ig) 施用 0.015 mL/g 10% v/v 乙醇溶液和同时使用纳米姜黄素对 21 日龄后代 Wistar 大鼠前额叶的影响皮层参数。评估了 CYP2E1、DBN1、DNMT1、miRNA-335、miRNA-21、c-Fos 和 Cox-2 基因表达以及伴随的组织学和超微结构改变。实施的实验设置表明，乙醇暴露导致上述参数发生显着变化。当纳米姜黄素同时给药时，在纳米姜黄素治疗的动物中观察到的变化与乙醇治疗组有显着差异。