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 2.4 3区 医学 Q2 PSYCHOLOGY
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。
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来源期刊
CiteScore
4.80
自引率
5.90%
发文量
224
审稿时长
3 months
期刊介绍: The Journal of Studies on Alcohol and Drugs began in 1940 as the Quarterly Journal of Studies on Alcohol. It was founded by Howard W. Haggard, M.D., director of Yale University’s Laboratory of Applied Physiology. Dr. Haggard was a physiologist studying the effects of alcohol on the body, and he started the Journal as a way to publish the increasing amount of research on alcohol use, abuse, and treatment that emerged from Yale and other institutions in the years following the repeal of Prohibition in 1933. In addition to original research, the Journal also published abstracts summarizing other published documents dealing with alcohol. At Yale, Dr. Haggard built a large team of alcohol researchers within the Laboratory of Applied Physiology—including E.M. Jellinek, who became managing editor of the Journal in 1941. In 1943, to bring together the various alcohol research projects conducted by the Laboratory, Dr. Haggard formed the Section of Studies on Alcohol, which also became home to the Journal and its editorial staff. In 1950, the Section was renamed the Center of Alcohol Studies.
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