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桑色素通过改善氧化应激和神经炎症减轻阿尔茨海默病大鼠模型的记忆缺陷。

Morin attenuates memory deficits in a rat model of Alzheimer's disease by ameliorating oxidative stress and neuroinflammation.

作者信息

Mohammadi Negin, Asle-Rousta Masoumeh, Rahnema Mehdi, Amini Rahim

机构信息

Department of Physiology, Zanjan Branch, Islamic Azad University, Zanjan, Iran.

Department of Physiology, Zanjan Branch, Islamic Azad University, Zanjan, Iran.

出版信息

Eur J Pharmacol. 2021 Nov 5;910:174506. doi: 10.1016/j.ejphar.2021.174506. Epub 2021 Sep 14.

DOI:10.1016/j.ejphar.2021.174506
PMID:34534533
Abstract

This study aimed to investigate the effect of flavonoid morin on oxidative/nitrosative stress, neuroinflammation, and histological, molecular, and behavioral changes caused by amyloid-beta (Aβ) in male Wistar rats (Alzheimer's disease model). Rats received morin (20 mg/kg, oral gavage) for 14 consecutive days after intrahippocampal injection of Aβ. Morin decreased the levels of malondialdehyde and nitric oxide, increased glutathione content, and enhanced catalase activity in the hippocampus of animals receiving Aβ. It also reduced the expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, nuclear factor-kappa B, and N-methyl-D-aspartate receptor subunits 2A and 2B and increased the expression of brain-derived neurotrophic factor and α7 nicotinic acetylcholine receptor in the hippocampus of Aβ-injected rats. Besides, morin modified neuronal loss and histological changes in the CA1 region of the hippocampus. Morin allowed Aβ-infused rats to swim more time in the target quadrant in the Morris water maze test. It is concluded that morin may be suitable for the prevention and treatment of Alzheimer's disease by strengthening the antioxidant system, inhibiting neuroinflammation, preventing neuronal death, and enhancing memory function.

摘要

本研究旨在探讨黄酮类化合物桑色素对雄性Wistar大鼠(阿尔茨海默病模型)中由β-淀粉样蛋白(Aβ)引起的氧化/亚硝化应激、神经炎症以及组织学、分子和行为变化的影响。在海马内注射Aβ后,大鼠连续14天接受桑色素(20毫克/千克,灌胃)。桑色素降低了接受Aβ的动物海马中丙二醛和一氧化氮的水平,增加了谷胱甘肽含量,并增强了过氧化氢酶活性。它还降低了肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6、核因子-κB以及N-甲基-D-天冬氨酸受体亚基2A和2B的表达,并增加了注射Aβ大鼠海马中脑源性神经营养因子和α7烟碱型乙酰胆碱受体的表达。此外,桑色素改善了海马CA1区的神经元丢失和组织学变化。在莫里斯水迷宫试验中,桑色素使注入Aβ的大鼠在目标象限游泳的时间更长。得出的结论是,桑色素可能通过加强抗氧化系统、抑制神经炎症、预防神经元死亡和增强记忆功能而适用于阿尔茨海默病的预防和治疗。

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