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山姜酮对淀粉样蛋白-β诱导的认知障碍的神经保护作用。

Neuroprotective effects of nootkatone from Alpiniae oxyphyllae Fructus against amyloid-β-induced cognitive impairment.

机构信息

Faculty of Functional Food and Wine, Shenyang Pharmaceutical University, Wenhua Road 103, Shenyang, 110016, People's Republic of China.

Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang, People's Republic of China.

出版信息

Metab Brain Dis. 2018 Feb;33(1):251-259. doi: 10.1007/s11011-017-0154-6. Epub 2017 Nov 24.

DOI:10.1007/s11011-017-0154-6
PMID:29177693
Abstract

The sesquiterpene nootkatone (NKT), isolated from Alpiniae oxyphyllae Fructus, was shown to possess protective effects on neurons. In our study, by using an Alzheimer's disease (AD) model of mice induced by intracerebroventricular (i.c.v.) injection of Aβ oligomers, we investigated the effects of NKT on memory impairment and further evaluated the pathological changes of mice. AD mice were treated by i.c.v. injection of NKT (at a dose of 0.02 mg/kg and 0.20 mg/kg) or vehicle (PBS) into the lateral ventricle once daily for 5 consecutive days. The behavioral tasks were performed, and levels of some biochemical indicators and histopathological changes of the brain were evaluated to elucidate the mechanism of NKT in the treatment of AD. The results revealed that NKT significantly improved the neurobehavioral performance of the AD mice in the Y-maze and Morris water maze tests. More importantly, NKT treatment decreased the malondialdehyde (MDA), Aβ as well as the acetylcholin esterase (AChE) levels in the mice brain, while increased the glutathione peroxidase (GSH-Px) levels with improved histopathological changes in the hippocampus. These findings provided evidences for the beneficial role of NKT in Aβ-induced mice AD model linking to anti-oxidative and anti-AChE activities with inhibitory effect against Aβ accumulation.

摘要

从益智果实中分离得到的倍半萜诺卡酮(NKT)被证明对神经元具有保护作用。在我们的研究中,通过使用脑室内(i.c.v.)注射 Aβ 寡聚体诱导的阿尔茨海默病(AD)小鼠模型,我们研究了 NKT 对记忆障碍的影响,并进一步评估了小鼠的病理变化。AD 小鼠通过 i.c.v. 注射 NKT(剂量为 0.02 mg/kg 和 0.20 mg/kg)或载体(PBS)到侧脑室,每天一次,连续 5 天。进行行为任务,并评估一些生化指标和脑组织的组织病理学变化,以阐明 NKT 在 AD 治疗中的作用机制。结果表明,NKT 显著改善了 AD 小鼠在 Y 迷宫和 Morris 水迷宫测试中的神经行为表现。更重要的是,NKT 治疗降低了小鼠大脑中的丙二醛(MDA)、Aβ 以及乙酰胆碱酯酶(AChE)水平,同时增加了谷胱甘肽过氧化物酶(GSH-Px)水平,并改善了海马的组织病理学变化。这些发现为 NKT 在 Aβ 诱导的 AD 模型小鼠中的有益作用提供了证据,与抗氧化和抗 AChE 活性以及抑制 Aβ 积累有关。

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