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利用多模式作用的绿茶儿茶素靶向多种神经退行性疾病病因。

Targeting multiple neurodegenerative diseases etiologies with multimodal-acting green tea catechins.

作者信息

Mandel Silvia A, Amit Tamar, Kalfon Limor, Reznichenko Lydia, Youdim Moussa B H

机构信息

Eve Topf Center for Neurodegenerative Diseases Research and Department of Pharmacology, Faculty of Medicine, Technion, Haifa, Israel.

出版信息

J Nutr. 2008 Aug;138(8):1578S-1583S. doi: 10.1093/jn/138.8.1578S.

Abstract

Green tea is currently considered a source of dietary constituents endowed with biological and pharmacological activities relevant to human health. Human epidemiological and new animal data suggest that the pharmacological benefits of tea drinking may help to protect the brain as we age. Indeed, tea consumption is inversely correlated with the incidence of dementia and Alzheimer's and Parkinson's diseases. In particular, its main catechin polyphenol constituent (-)-epigallocatechin-3-gallate has been shown to exert neuroprotective/neurorescue activities in a wide array of cellular and animal models of neurological disorders. The intense efforts dedicated in recent years to shed light on the molecular mechanisms participating in the brain protective action of green tea indicate that in addition to the known antioxidant activity of catechins, the modulation of signal transduction pathways, cell survival/death genes, and mitochondrial function all contribute significantly to the induction of neuron viability. Because of the multietiological character of neurodegenerative disease pathology, these natural compounds are receiving significant attention as therapeutic cytoprotective agents that simultaneously manipulate multiple desired targets in the central nervous system. This article elaborates on the multimodal activities of green tea polyphenols with emphasis on their recently described neurorescue/neuroregenerative and mitochondrial stabilization actions.

摘要

绿茶目前被认为是一种膳食成分来源,其所含的生物和药理活性与人类健康相关。人类流行病学和新的动物数据表明,随着年龄增长,饮茶的药理益处可能有助于保护大脑。事实上,茶的摄入量与痴呆症、阿尔茨海默病和帕金森病的发病率呈负相关。特别是,其主要的儿茶素多酚成分(-)-表没食子儿茶素-3-没食子酸酯已被证明在多种神经疾病的细胞和动物模型中发挥神经保护/神经挽救作用。近年来,人们致力于阐明参与绿茶脑保护作用的分子机制,结果表明,除了儿茶素已知的抗氧化活性外,信号转导通路、细胞存活/死亡基因和线粒体功能的调节均对神经元活力的诱导有显著贡献。由于神经退行性疾病病理具有多病因特征,这些天然化合物作为能同时调控中枢神经系统多个理想靶点的治疗性细胞保护剂正受到广泛关注。本文详细阐述了绿茶多酚的多模式活性,重点介绍了其最近描述的神经挽救/神经再生和线粒体稳定作用。

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