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辣木减轻 APP/PS1 小鼠的 Aβ 负担并改善突触可塑性和认知障碍。

Moringa Oleifera Alleviates Aβ Burden and Improves Synaptic Plasticity and Cognitive Impairments in APP/PS1 Mice.

机构信息

Co-Innovation Center of Neuroregeneration, Nantong University, Nantong 226001, China.

Cognitive Impairment Ward of Neurology Department, The Third Affiliated Hospital of Shenzhen University, 47 Youyi Rd., Shenzhen 518001, China.

出版信息

Nutrients. 2022 Oct 14;14(20):4284. doi: 10.3390/nu14204284.

DOI:10.3390/nu14204284
PMID:36296969
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9609596/
Abstract

Alzheimer's disease is a global public health problem and the most common form of dementia. Due to the failure of many single therapies targeting the two hallmarks, Aβ and Tau, and the multifactorial etiology of AD, there is now more and more interest in nutraceutical agents with multiple effects such as (MO) that have strong anti-oxidative, anti-inflammatory, anticholinesterase, and neuroprotective virtues. In this study, we treated APP/PS1 mice with a methanolic extract of MO for four months and evaluated its effect on AD-related pathology in these mice using a multitude of behavioral, biochemical, and histochemical tests. Our data revealed that MO improved behavioral deficits such as anxiety-like behavior and hyperactivity and cognitive, learning, and memory impairments. MO treatment abrogated the Aβ burden to wild-type control mice levels via decreasing BACE1 and AEP and upregulating IDE, NEP, and LRP1 protein levels. Moreover, MO improved synaptic plasticity by improving the decreased GluN2B phosphorylation, the synapse-related proteins PSD95 and synapsin1 levels, the quantity and quality of dendritic spines, and neurodegeneration in the treated mice. MO is a nutraceutical agent with promising therapeutic potential that can be used in the management of AD and other neurodegenerative diseases.

摘要

阿尔茨海默病是一个全球性的公共卫生问题,也是最常见的痴呆症形式。由于许多针对 Aβ 和 Tau 这两个标志性特征的单一疗法都失败了,而且 AD 的病因是多因素的,因此现在越来越多的人对具有多种作用的营养药物(MO)感兴趣,这些药物具有很强的抗氧化、抗炎、抗胆碱酯酶和神经保护作用。在这项研究中,我们用 MO 的甲醇提取物治疗 APP/PS1 小鼠四个月,并使用多种行为、生化和组织化学测试来评估其对这些小鼠的 AD 相关病理的影响。我们的数据显示,MO 通过降低 BACE1 和 AEP 并上调 IDE、NEP 和 LRP1 蛋白水平,改善了焦虑样行为和过度活跃以及认知、学习和记忆障碍等行为缺陷。此外,MO 通过改善减少的 GluN2B 磷酸化、突触相关蛋白 PSD95 和突触素 1 水平、树突棘的数量和质量以及治疗小鼠中的神经退行性变,改善了突触可塑性。MO 是一种具有广阔治疗潜力的营养药物,可用于 AD 和其他神经退行性疾病的治疗。

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