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维生素 E 可改善高脂肪饮食诱导的大鼠惊厥阈降低:氧化应激的作用。

Vitamin E modifies high-fat diet-induced reduction of seizure threshold in rats: Role of oxidative stress.

机构信息

Department of Clinical Pharmacy, Jordan University of Science and Technology, Irbid, Jordan.

Department of Physiology, College of Medicine and Medical Sciences, Arabian Gulf University, Manama, Bahrain.

出版信息

Physiol Behav. 2019 Jul 1;206:200-205. doi: 10.1016/j.physbeh.2019.04.011. Epub 2019 Apr 13.

Abstract

There is increasing evidence that oxidative stress is a causal factor in different neurodegenerative disorders such as Alzheimer's disease and epilepsy. High-fat diet (HFD) has been shown to induce oxidative stress and neuronal damage that may increase susceptibility to seizures. The present study was undertaken to investigate the relationships between vitamin E, a potent antioxidant, HFD, and chemically induced seizures, using the PTZ seizure model in rats. Animals were randomly assigned into four groups: control, HFD, vitamin E (Vit E), and high-fat diet with vitamin E (HFD + Vit E) group. Vitamin E and/or HFD were administered to animals for 6 weeks. Thereafter, PTZ seizure threshold was measured in control and treated rats, and different brain regions were analyzed for levels of oxidative stress biomarkers. Current results revealed a significant reduction in PTZ seizure threshold in rats consuming HFD, which could be prevented by vitamin E supplement. Alongside, vitamin E supplement prevented HFD induced changes in oxidative stress biomarkers and capacity enzymes. Therefore, current results suggest that prolonged consumption of HFD increases susceptibility to PTZ induced seizures, which may be related to HFD induced oxidative stress. This increase in the PTZ susceptibility could be prevented by the administration of vitamin E, probably through its antioxidant effect, particularly at the brain hippocampal region.

摘要

越来越多的证据表明,氧化应激是阿尔茨海默病和癫痫等不同神经退行性疾病的一个因果因素。高脂肪饮食(HFD)已被证明会引起氧化应激和神经元损伤,从而增加癫痫发作的易感性。本研究旨在使用大鼠 PTZ 癫痫模型,研究维生素 E(一种有效的抗氧化剂)、HFD 和化学诱导性癫痫之间的关系。动物被随机分为四组:对照组、HFD 组、维生素 E(Vit E)组和 HFD+维生素 E(HFD+Vit E)组。维生素 E 和/或 HFD 给予动物 6 周。此后,在对照组和治疗组大鼠中测量 PTZ 癫痫发作阈值,并分析不同脑区的氧化应激生物标志物水平。目前的结果表明,食用 HFD 的大鼠的 PTZ 癫痫发作阈值显著降低,而维生素 E 补充可以预防这种降低。此外,维生素 E 补充可防止 HFD 诱导的氧化应激生物标志物和能力酶的变化。因此,目前的结果表明,长期食用 HFD 会增加对 PTZ 诱导的癫痫发作的易感性,这可能与 HFD 诱导的氧化应激有关。通过给予维生素 E,可以预防这种对 PTZ 敏感性的增加,这可能是通过其抗氧化作用,特别是在大脑海马区。

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