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柠檬精油通过调节海马突触密度和抑制乙酰胆碱酯酶改善与年龄相关的认知功能障碍。

Lemon essential oil ameliorates age-associated cognitive dysfunction via modulating hippocampal synaptic density and inhibiting acetylcholinesterase.

机构信息

Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin 150081, China.

Basic Medical Institute of Heilongjiang Medical Science Academy, Harbin 150081, China.

出版信息

Aging (Albany NY). 2020 May 11;12(9):8622-8639. doi: 10.18632/aging.103179.

DOI:10.18632/aging.103179
PMID:32392535
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7244039/
Abstract

The lemon essential oil (LEO), extracted from the fruit of lemon, has been used to treat multiple pathological diseases, such as diabetes, inflammation, cardiovascular diseases, depression and hepatobiliary dysfunction. The study was designed to study the effects of LEO on cognitive dysfunction induced by Alzheimer's disease (AD). We used APP/PS1 double transgene (APP/PS1) AD mice in the experiment; these mice exhibit significant deficits in synaptic density and hippocampal-dependent spatial related memory. The effects of LEO on learning and memory were examined using the Morris Water Maze (MWM) test, Novel object recognition test, and correlative indicators, including a neurotransmitter (acetylcholinesterase, AChE), a nerve growth factor (brain-derived neurotrophic factor, BDNF), a postsynaptic marker (PSD95), and presynaptic markers (synapsin-1, and synaptophysin), in APP/PS1 mice. Histopathology was performed to estimate the effects of LEO on AD mice. A significantly lowered brain AChE depression in APP/PS1 and wild-type C57BL/6L (WT) mice. PSD95/ Synaptophysin, the index of synaptic density, was noticeably improved in histopathologic changes. Hence, it can be summarized that memory-enhancing activity might be associated with a reduction in the AChE levels and is elevated by BDNF, PSD95, and synaptophysin through enhancing synaptic plasticity.

摘要

柠檬精油(LEO)从柠檬果实中提取,已用于治疗多种病理疾病,如糖尿病、炎症、心血管疾病、抑郁症和肝胆功能障碍。本研究旨在研究柠檬精油对阿尔茨海默病(AD)引起的认知功能障碍的影响。我们在实验中使用了 APP/PS1 双转基因(APP/PS1)AD 小鼠;这些小鼠表现出突触密度和海马依赖性空间相关记忆显著缺陷。通过 Morris 水迷宫(MWM)测试、新物体识别测试以及相关指标(包括神经递质(乙酰胆碱酯酶,AChE)、神经生长因子(脑源性神经营养因子,BDNF)、突触后标记物(PSD95)和突触前标记物(突触素-1 和突触小体))来检查 LEO 对 APP/PS1 小鼠的学习和记忆的影响。进行组织病理学检查以评估 LEO 对 AD 小鼠的影响。APP/PS1 和野生型 C57BL/6L(WT)小鼠的脑 AChE 降低明显降低。突触密度的指标 PSD95/Synaptophysin 在组织病理学变化中明显改善。因此,可以总结出,增强记忆的活性可能与 AChE 水平降低有关,并通过 BDNF、PSD95 和突触小体来提高,从而增强突触可塑性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603e/7244039/af034dd892e7/aging-12-103179-g007.jpg
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