Epigallocatechin-3-Gallate Inhibits Oxidative Stress Through the Keap1/Nrf2 Signaling Pathway to Improve Alzheimer Disease.

IF 4.6 2区 医学 Q1 NEUROSCIENCES Molecular Neurobiology Pub Date : 2025-03-01 Epub Date: 2024-09-20 DOI:10.1007/s12035-024-04498-6
Shi Tang, Yong Zhang, Benson O A Botchway, Xichen Wang, Min Huang, Xuehong Liu
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Abstract

Alzheimer disease (AD) is a common neurodegenerative disease with an intricate pathophysiological mechanism. Oxidative stress has been shown in several investigations as a significant factor in AD progression. For instance, studies have confirmed that oxidative stress inhibition may considerably improve AD symptoms, with potent antioxidants being touted as a possible interventional strategy in the search for AD treatment. Epigallocatechin-3-gallate (EGCG) acts as a natural catechin that has antioxidant effect. It activates the kelch-like epichlorohydrin-associated proteins (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway to inhibit oxidative stress. The Keap1/Nrf2 signal pathway is not only an upstream signaling target for a variety of antioxidant enzymes, but also minimizes high levels of reactive oxygen species. This report analyzes the antioxidant effect of EGCG in AD, elaborates its specific mechanism of action, and provides a theoretical basis for its clinical application in AD.

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表没食子儿茶素-3-棓酸盐通过 Keap1/Nrf2 信号通路抑制氧化应激以改善阿尔茨海默病
阿尔茨海默病(AD)是一种常见的神经退行性疾病,其病理生理机制错综复杂。多项研究表明,氧化应激是导致阿尔茨海默病恶化的重要因素。例如,研究证实,抑制氧化应激可大大改善阿兹海默症的症状,强效抗氧化剂被认为是寻找阿兹海默症治疗方法的一种可能的干预策略。表没食子儿茶素-3-棓酸盐(EGCG)是一种具有抗氧化作用的天然儿茶素。它能激活类开尔奇环氧氯丙烷相关蛋白(Keap1)/核因子红细胞2相关因子2(Nrf2)信号通路,从而抑制氧化应激。Keap1/Nrf2信号通路不仅是多种抗氧化酶的上游信号靶点,还能将高水平的活性氧降至最低。本报告分析了EGCG在AD中的抗氧化作用,阐述了其具体的作用机制,并为其在AD中的临床应用提供了理论依据。
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来源期刊
Molecular Neurobiology
Molecular Neurobiology 医学-神经科学
CiteScore
9.00
自引率
2.00%
发文量
480
审稿时长
1 months
期刊介绍: Molecular Neurobiology is an exciting journal for neuroscientists needing to stay in close touch with progress at the forefront of molecular brain research today. It is an especially important periodical for graduate students and "postdocs," specifically designed to synthesize and critically assess research trends for all neuroscientists hoping to stay active at the cutting edge of this dramatically developing area. This journal has proven to be crucial in departmental libraries, serving as essential reading for every committed neuroscientist who is striving to keep abreast of all rapid developments in a forefront field. Most recent significant advances in experimental and clinical neuroscience have been occurring at the molecular level. Until now, there has been no journal devoted to looking closely at this fragmented literature in a critical, coherent fashion. Each submission is thoroughly analyzed by scientists and clinicians internationally renowned for their special competence in the areas treated.
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