鞣花酸 (EA) 具有神经保护、线粒体保护、抗氧化和抗炎作用。我们评估了电针对乙醇诱导的胎儿酒精谱系障碍 (FASD) 的保护作用。总共使用 35 只新生雄性大鼠，分为 5 组，包括：对照（生理盐水）、乙醇（5.25 g/kg/天）、乙醇（5.25 g/kg/天）EA（10 mg/kg）、乙醇（5.25 g/kg/天）EA（20 mg/kg）和乙醇（每天 5.25 克/公斤） EA（40 毫克/公斤）。出生后36天行为测试（Morris水迷宫和高架十字迷宫）、肿瘤坏死因子-α（TNF-α）水平、氧化标记物（丙二醛、谷胱甘肽和超氧化物歧化酶）、线粒体检查如琥珀酸脱氢酶（SDH）分析了线粒体活性、线粒体肿胀、线粒体膜电位（MMP）和活性氧（ROS）形成。结果表明，乙醇暴露会对认知和线粒体功能产生不利影响，并诱发脑组织氧化应激和炎症。然而，EA（20 和 40 mg/kg）给药有效预防了 FASD 模型中乙醇的毒性作用。这些研究结果表明，乙醇的应用通过线粒体功能障碍和诱导氧化应激显着损害大脑发育。这些数据表明 EA 可能是预防酒精引起的 FASD 的有用化合物。

Ellagic acid (EA) exerts, neuroprotective, mitoprotective, anti-oxidative and anti-inflammatory effects. We evaluated protective effect of EA on ethanol-induced fetal alcohol spectrum disorders (FASD).A total of 35 newborn male rats were used, divided into five groups, including; control (normal saline), ethanol (5.25 g/kg per day), ethanol (5.25 g/kg per day) + EA (10 mg/kg), ethanol (5.25 g/kg per day) + EA (20 mg/kg) and ethanol (5.25 g/kg per day) + EA (40 mg/kg). Thirty-six days after birth behavioral tests (Morris water maze and Elevated Plus Maze), tumor necrosis factor-α (TNF-α) levels, oxidative markers (malondialdehyde, glutathione and superoxide dismutase), mitochondrial examination such as succinate dehydrogenases (SDH) activity, mitochondrial swelling, mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) formation were analyzed.The results revealed that ethanol exposure adversely affected cognitive and mitochondrial functions and as well as induced oxidative stress and inflammation in brain tissue. However, EA (20 and 40 mg/kg) administration effectively prevented the toxic effects of ethanol in FASD model.These findings demonstrate that ethanol application significantly impairs the brain development via mitochondrial dysfunction and induction of oxidative stress. These data indicate that EA might be a useful compound for prevention of alcohol-induced FASD.