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ergothioneine 可预防β-淀粉样蛋白诱导的小鼠神经元损伤。

Ergothioneine protects against neuronal injury induced by β-amyloid in mice.

机构信息

School of Nutrition, Chung Shan Medical University and Department of Nutrition, Chung Shan Medical University Hospital, Taichung, Taiwan, ROC.

出版信息

Food Chem Toxicol. 2012 Nov;50(11):3902-11. doi: 10.1016/j.fct.2012.08.021. Epub 2012 Aug 16.

DOI:10.1016/j.fct.2012.08.021
PMID:22921351
Abstract

β-Amyloid peptides (Aβ) are neurotoxic and contribute to the development of Alzheimer's disease (AD). Ergothioneine (EGT) has been shown to protect against loss of memory and learning abilities in mice. In this study, mice were orally fed EGT (0.5 or 2 mg/kg body weight) for 16 days before treatment (i.c.v) with a single dose of Aβ1-40 in the hippocampus. After resting for 12 days to restore the body weight, the mice were again fed EGT for additional 39 days. Active avoidance tests were conducted on days 37-39 (short-memory avoidance) and on days 37, 44 and 51 (long-memory avoidance). Water maze task was used to evaluate learning and memory abilities by acquisition test and retention test. In both long-memory avoidance and water maze tests, EGT significantly decreased the escape latency and increased the frequency of successful avoidance. Furthermore, EGT significantly prevented Aβ accumulation in the hippocampus and brain lipid peroxidation, restored acetylcholinesterase (AChE) activity, maintained glutathione/glutathione disulfide ratio and superoxide dismutase activity in brain tissues of Aβ1-40-teated mice. Thus, EGT can protect against Aβ-induced loss of memory and learning abilities in mice. Further studies are required to confirm the protective effects of EGT on the development or progression of AD.

摘要

β-淀粉样肽(Aβ)具有神经毒性,是导致阿尔茨海默病(AD)发生的原因之一。已证实,麦硫因(EGT)可保护小鼠免受记忆和学习能力丧失的影响。在这项研究中,将 Aβ1-40 单次侧脑室注射到小鼠海马体中之前,用 EGT(0.5 或 2mg/kg 体重)对其进行 16 天的口服喂养。在恢复体重 12 天后,再次给予 EGT 喂养 39 天。在第 37-39 天(短期记忆回避)和第 37、44 和 51 天(长期记忆回避)进行主动回避测试。水迷宫任务用于通过获得测试和保留测试来评估学习和记忆能力。在长时记忆回避和水迷宫测试中,EGT 均显著降低逃避潜伏期并增加成功回避的频率。此外,EGT 可显著防止 Aβ在海马体中的积累和脑脂质过氧化,恢复乙酰胆碱酯酶(AChE)活性,维持脑组织中谷胱甘肽/谷胱甘肽二硫化物比和超氧化物歧化酶活性。因此,EGT 可保护小鼠免受 Aβ诱导的记忆和学习能力丧失的影响。需要进一步的研究来确认 EGT 对 AD 的发展或进展的保护作用。

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