Myricetin ameliorates scopolamine-induced memory impairment in mice via inhibiting acetylcholinesterase and down-regulating brain iron.
Myricetin ameliorates scopolamine-induced memory impairment in mice via inhibiting acetylcholinesterase and down-regulating brain iron.
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DOI：
10.1016/j.bbrc.2017.06.045
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发表时间：
2017-08
影响因子：
3.1
通讯作者：
Beiyun Wang;Y. Zhong;Chengjie Gao;Jingbo Li
中科院分区：
文献类型：
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作者：
Beiyun Wang;Y. Zhong;Chengjie Gao;Jingbo Li
本研究旨在探讨杨梅素对阿尔茨海默病（AD）的治疗作用及其机制。在我们的研究中，杨梅素有效地减弱了Fe ~（2+）诱导的SH-SY 5 Y细胞死亡。在AD小鼠模型中，杨梅素治疗显著逆转东莨菪碱诱导的认知缺陷，其来源于抑制乙酰胆碱酯酶（AChE）和下调脑铁的新作用。此外，杨梅素治疗减少了小鼠的氧化损伤，增加了抗氧化酶的活性。有趣的是，杨梅素的作用在很大程度上被高铁饮食所消除。因此，我们认为，用杨梅素治疗可以减轻小鼠的认知缺陷，抑制AChE和脑铁调节。此外，杨梅素降低铁含量可能通过抑制转铁蛋白受体1（TrR 1）表达。总之，积累的数据表明，杨梅素是一个潜在的多功能药物治疗AD。
The aim of our study was to investigate to investigate the effect of myricetin on Alzheimer's disease (AD) and its underlying mechanisms. In our study, Myricetin effectively attenuated Fe2+-induced cell death in SH-SY5Y cellsin vitro. In a mouse model of AD, myricetin treatment significantly reversed scopolamine-induced cognitive deficits deriving from a novel action of inhibiting acetylcholinesterase (AChE) and down-regulating brain iron. Furthermore, Myricetin treatment reduced oxidative damage and increased antioxidant enzymes activity in mice. Interestingly, the effect of myricetin was largely abolished by high iron diet. Therefore we suggested that treatment with myricetin attenuated cognitive deficits in miceviainhibiting AChE and brain iron regulation. In addition, myricetin reduce iron contents mayviainhibiting transferrin receptor 1 (TrR1) expression. In conclusion, accumulated data demonstrates that myricetin is a potential multifunctional drug for AD.