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膳食多酚对神经毒性β-淀粉样蛋白的保护作用:从分子到临床。

Dietary polyphenol-derived protection against neurotoxic β-amyloid protein: from molecular to clinical.

机构信息

Discipline of Pharmacology, School of Medical Sciences, Faculty of Health Sciences, The University of Adelaide, South Australia.

出版信息

Food Funct. 2012 Dec;3(12):1242-50. doi: 10.1039/c2fo30075c.

DOI:10.1039/c2fo30075c
PMID:22929970
Abstract

Polyphenolic compounds derived mainly from plant products have demonstrated neuroprotective properties in a number of experimental settings. Such protective effects have often been ascribed to antioxidant capacity, but specific augmentation of other cellular defences and direct interactions with neurotoxic proteins have also been demonstrated. With an emphasis on neurodegenerative conditions, such as Alzheimer's disease, we highlight recent findings on the neuroprotection ascribed to bioactive polyphenols capable of directly interfering with the Alzheimer's disease hallmark toxic β-amyloid protein (Aβ), thereby inhibiting fibril and aggregate formation. This includes compounds such as the green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) and the phytoalexin resveratrol. Targeted studies on the biomolecular interactions between dietary polyphenolics and Aβ have not only improved our understanding of the pathogenic role of β-amyloid, but also offer fundamentally novel treatment options for Alzheimer's disease and potentially other amyloidoses.

摘要

多酚化合物主要来源于植物产品,在许多实验环境中表现出神经保护特性。这种保护作用通常归因于抗氧化能力,但也证明了对其他细胞防御的特定增强以及与神经毒性蛋白的直接相互作用。我们强调了神经退行性疾病(如阿尔茨海默病)的情况,突出了最近关于生物活性多酚的神经保护作用的发现,这些多酚能够直接干扰阿尔茨海默病标志性的有毒β-淀粉样蛋白(Aβ),从而抑制纤维和聚集体的形成。这包括绿茶多酚(-)-表没食子儿茶素-3-没食子酸酯(EGCG)和植物抗毒素白藜芦醇等化合物。针对膳食多酚和 Aβ 之间的生物分子相互作用的靶向研究不仅提高了我们对β-淀粉样蛋白致病作用的理解,而且为阿尔茨海默病及潜在的其他淀粉样变性病提供了从根本上新颖的治疗选择。

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