Protective Role of Ellagic Acid Against Ethanol-Induced Neurodevelopmental Disorders in Newborn Male Rats: Insights into Maintenance of Mitochondrial Function and Inhibition of Oxidative Stress.

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Zhaleh Jamali, Ahmad Salimi, Saleh Khezri, Pirasteh Norozi, Behzad Garmabi, Mehdi Khaksari
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Abstract

Objective: 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).

Methods: 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.

Results: 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.

Conclusions: 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.

鞣花酸对乙醇诱导的新生雄性大鼠神经发育障碍的保护作用:对维持线粒体功能和抑制氧化应激的启示
目的:鞣花酸(EA)具有神经保护、有丝分裂保护、抗氧化和抗炎作用:鞣花酸(EA)具有神经保护、有丝分裂保护、抗氧化和抗炎作用。我们评估了鞣花酸对乙醇诱导的胎儿酒精谱系障碍(FASD)的保护作用:共使用 35 只新生雄性大鼠,分为五组,包括:对照组(生理盐水)、乙醇组(每天 5.25 克/千克)、乙醇组(每天 5.25 克/千克)+EA 组(10 毫克/千克)、乙醇组(每天 5.25 克/千克)+EA 组(20 毫克/千克)和乙醇组(每天 5.25 克/千克)+EA 组(40 毫克/千克)。对小鼠出生后36天的行为测试(莫里斯水迷宫和高架加迷宫)、肿瘤坏死因子-α(TNF-α)水平、氧化指标(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)活性)、线粒体肿胀、线粒体膜电位(MMP)和活性氧(ROS)形成进行了分析: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 毫克和 40 毫克/千克)能有效防止乙醇对 FASD 模型的毒性作用:这些研究结果表明,应用乙醇会通过线粒体功能障碍和诱导氧化应激显著损害大脑发育。这些数据表明,EA 可能是预防酒精诱发 FASD 的有效化合物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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