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评价硒对睡眠剥夺引起的空间记忆障碍的影响。

Evaluating the effect of selenium on spatial memory impairment induced by sleep deprivation.

机构信息

Department of Medicinal Chemistry and Pharmacognosy , Faculty of Pharmacy, Jordan University of Science and Technology, P.O. Box 3030, Irbid 22110 Jordan.

Department of Pharmacy Practice and Pharmacotherapeutics, University of Sharjah, Sharjah, UAE; Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, P.O. Box 3030, Irbid 22110 Jordan.

出版信息

Physiol Behav. 2022 Feb 1;244:113669. doi: 10.1016/j.physbeh.2021.113669. Epub 2021 Dec 3.

Abstract

Sleep deprivation (SD) impairs memory due to disturbing oxidative stress parameters. Selenium is a main component of several antioxidant enzymes and provides a neuroprotective effect. The present study aimed to investigate the potential neuroprotective effect of chronic selenium administration on cognitive impairments induced by chronic SD. Adult male Wister rats were randomly assigned into five groups (n = 12/group). The SD was induced in rats using modified multiple platform model. Selenium (6 µg/kg of animal's body weight) was administered to rats via oral gavage for 6 weeks. The spatial learning and memory were assessed using the radial arm water maze (RAWM). Moreover, we measured the levels of reduced glutathione (GSH), oxidized glutathione (GSSG) and GSH/GSSG, catalase, glutathione peroxidase (GPx), superoxide dismutase (SOD), thiobarbituric acid reactive substances (TBARS) and brain derived neurotrophic factor (BDNF) in the hippocampus. The results indicate that short- and long-term memory were impaired by chronic sleep deprivation (P < 0.05), while selenium administration prevented this effect. Moreover, selenium normalized antioxidants activities which were reduced by SD such as: catalase (P < 0.05), and SOD (P < 0.05), and significantly enhanced the ratio of GSH/GSSG in sleep-deprived rats (P < 0.05), without significant alteration of BDNF (P > 0.05), GSH (P > 0.05), or TBARS levels (P > 0.05). In conclusion, chronic SD induced memory impairment, and chronic treatment with selenium prevented this impairment by normalizing antioxidant enzymes activities in the hippocampus.

摘要

睡眠剥夺(SD)会破坏氧化应激参数,从而损害记忆。硒是几种抗氧化酶的主要成分,具有神经保护作用。本研究旨在探讨慢性硒给药对慢性 SD 诱导的认知障碍的潜在神经保护作用。成年雄性 Wistar 大鼠随机分为五组(每组 n = 12)。使用改良的多平台模型诱导大鼠 SD。通过口服灌胃向大鼠给予硒(动物体重的 6μg/kg)6 周。使用放射臂水迷宫(RAWM)评估空间学习和记忆。此外,我们测量了海马中的还原型谷胱甘肽(GSH)、氧化型谷胱甘肽(GSSG)和 GSH/GSSG、过氧化氢酶、谷胱甘肽过氧化物酶(GPx)、超氧化物歧化酶(SOD)、硫代巴比妥酸反应物质(TBARS)和脑源性神经营养因子(BDNF)的水平。结果表明,慢性睡眠剥夺会损害短期和长期记忆(P<0.05),而硒给药可预防这种作用。此外,硒使 SD 降低的抗氧化剂活性正常化,如:过氧化氢酶(P<0.05)和 SOD(P<0.05),并显著增强睡眠剥夺大鼠的 GSH/GSSG 比值(P<0.05),而 BDNF(P>0.05)、GSH(P>0.05)或 TBARS 水平无明显变化(P>0.05)。总之,慢性 SD 引起记忆障碍,慢性硒治疗通过正常化海马中的抗氧化酶活性来预防这种障碍。

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