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大豆异黄酮对雄性 ICR 小鼠慢性乙醇诱导痴呆的神经保护作用。

Neuroprotective effects of soy isoflavones on chronic ethanol-induced dementia in male ICR mice.

机构信息

Institute of Food Science and Technology, Chinese Academy of Agricultural Sciences (CAAS), Beijing 100193, China.

出版信息

Food Funct. 2020 Nov 18;11(11):10011-10021. doi: 10.1039/d0fo02042g.

DOI:10.1039/d0fo02042g
PMID:33124635
Abstract

Chronic ethanol intake can lead to dementia by activating neuroinflammation, causing oxidative stress response, reducing cholinergic function and inducing neuronal apoptosis. Soy isoflavones (SIs) exert beneficial effects in a variety of neurodegenerative disorders by acting on the anti-inflammatory, anti-oxidant, anti-apoptotic and neuro-trophic processes. However, at present, it is unknown whether SIs have a neuroprotective effect in chronic ethanol-induced dementia. The aim of the present study was to investigate the effect of SI on chronic ethanol-induced cognitive deficit in mice and explore the underlying mechanisms. The cognition-impaired mouse model was induced by ethanol (2.0 g kg-1, p.o) for 4 weeks. SIs (10, 20 or 40 mg kg-1, p.o) were delivered 1 hour after ethanol administration for 4 weeks. The Morris water maze (MWM) test and the passive avoidance (PA) task were conducted to evaluate the learning and memory abilities. After the behavioral tests, the biochemical parameter assay and western blot analysis were used to explore the underlying mechanisms of its action. SI administration significantly improved the cognitive performance in the MWM and PA tests, regulated the acetylcholinesterase (AChE) activity and acetylcholine (Ach) level, elevated the synaptic plasticity-related protein expressions and inhibited neuron apoptosis-related protein expressions in the cortex and hippocampus of mice. The results revealed that soy isoflavones may provide a possible novel candidate for the prevention and treatment of alcoholic dementia.

摘要

慢性乙醇摄入可通过激活神经炎症、引起氧化应激反应、降低胆碱能功能和诱导神经元凋亡导致痴呆。大豆异黄酮(SIs)通过抗炎、抗氧化、抗凋亡和神经营养作用,对多种神经退行性疾病发挥有益作用。然而,目前尚不清楚 SIs 是否对慢性乙醇诱导的痴呆具有神经保护作用。本研究旨在探讨 SIs 对慢性乙醇诱导的小鼠认知障碍的影响,并探讨其潜在机制。采用乙醇(2.0 g/kg,口服)连续灌胃 4 周构建认知障碍小鼠模型。SIs(10、20 或 40 mg/kg,口服)在乙醇给药 1 小时后连续给药 4 周。通过 Morris 水迷宫(MWM)试验和被动回避(PA)试验评估学习和记忆能力。行为学测试后,采用生化参数测定和 Western blot 分析探讨其作用机制。SIs 给药可显著改善 MWM 和 PA 试验中的认知表现,调节乙酰胆碱酯酶(AChE)活性和乙酰胆碱(Ach)水平,提高皮质和海马中与突触可塑性相关的蛋白表达,抑制与神经元凋亡相关的蛋白表达。结果表明,大豆异黄酮可能为预防和治疗酒精性痴呆提供一种新的候选药物。

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