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维生素E对癫痫大鼠认知功能障碍的治疗作用及其可能机制
引用本文:修彬华,魏敏,李华,杨江河,闫志强,刘绍明.维生素E对癫痫大鼠认知功能障碍的治疗作用及其可能机制[J].生物磁学,2011(11):2094-2097.
作者姓名:修彬华  魏敏  李华  杨江河  闫志强  刘绍明
作者单位:兰州军区乌鲁木齐总医院神经外科,新疆乌鲁木齐830000
摘    要:目的:探讨维生素E(VitE)对癫痫大鼠认知功能障碍的治疗作用及其可能机制。方法:将30只成年雄性SD大鼠随机分为健康对照组、单纯致痫组(SE组)、VitE按体重100mg/(kg·d)]干预组(VitE组)。采用Morris水迷宫实验方法检测致癫后大鼠学习记忆功能变化,同时检测脑组织匀浆中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH—PX)、谷胱甘肽(GSH)、丙二醛(MDA)的水平。结果:(1)SE组大鼠寻找平台的潜伏期明显长于对照组,具有统计学意义(P〈0.05),VitE组寻找平台的潜伏期相对于SE组显著缩短(P〈0.05)。撤离平台后,SE组大鼠在平台所在象限的停留时间明显短于对照组(P〈0.05),VitE治疗后大鼠在平台所在象限的停留时间较SE组显著延长(P〈0.05)。(2)SE组SOD、GSH—PX、GSH显著下降,MDA明显增高,VitE干预组SOD、GSH.PX-GSH显著增高,而MDA明显下降,具有统计学意义(P〈0.05)。结论:VitE可改善癫痫持续状态后大鼠认知功能,其可能机制是通过减轻海马区的氧化应激反应减轻海马区的损伤,从而实现改善认知功能。

关 键 词:癫痫持续状态  维生素E  认知功能障碍

Vitamin E for Cognitive Dysfunction of Rats with Epilepsy
XIU Bin-hua,WEI Min,LI Hua,YANG Jiang-he,YAN Zhi-qiang,LIU Shao-ming.Vitamin E for Cognitive Dysfunction of Rats with Epilepsy[J].Biomagnetism,2011(11):2094-2097.
Authors:XIU Bin-hua  WEI Min  LI Hua  YANG Jiang-he  YAN Zhi-qiang  LIU Shao-ming
Affiliation:(Department of neurosurgery, Urumchi Hospital of Lanzhou Military region, Urumchi 830000, China)
Abstract:Objective: The purpose of the study was to investigate the effects of vitamin E (VitE) on cognitive deficits induced by status epilepticus (SE) and the possible mechanism in terms of oxidative stress in hippocampus. Methods: A total of 30 male Sprague-Dawley rats (200± 20 g) were randomly assigned to one of the following groups: (n =10 in each group): Control group,SE group and Vit E group. Severe cognitive deficits in lithium-pilocarpine seizure model was tested by the water maze task. Glutathione (GSH) and Maleic Dialdehyde(MDA) content of the homogenate of Hippocampus were measured; The activity of Superoxide Dismutase (SOD) and glutathione peroxidase (GSH-PX)in the homogenate of Hippocampus were detected. Results: Vitamin E could attenuate SE-induced cognitive deficits. Biochemical experiments revealed that SE can significantly increase content of MDA, decrease content of GSH and decreased the activities of SOD and GSH-PX in the homogenate of Hippocampus, which can be reversed by VitE. Conclusions: Vit E exhibits therapeutic potential for SE-induced cognitive deficits, which is most likely related, at least in part, to its anti-oxidative stress actions in hippocampus.
Keywords:Status epilepticus  Vitamin E  Cognitive deficits
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