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表没食子儿茶素-3-没食子酸酯通过Keap1/Nrf2信号通路抑制氧化应激以改善阿尔茨海默病。

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

作者信息

Tang Shi, Zhang Yong, Botchway Benson O A, Wang Xichen, Huang Min, Liu Xuehong

机构信息

Department of Histology and Embryology, School of Medicine, Shaoxing University, Shaoxing, 312000, China.

Bupa Cromwell Hospital, Kensington, London, UK.

出版信息

Mol Neurobiol. 2025 Mar;62(3):3493-3507. doi: 10.1007/s12035-024-04498-6. Epub 2024 Sep 20.

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.

摘要

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AD进展的一个重要因素。例如,研究证实抑制氧化应激可能会显著改善AD症状,强效抗氧化剂被认为是寻找AD治疗方法的一种可能的干预策略。表没食子儿茶素-3-没食子酸酯(EGCG)是一种具有抗氧化作用的天然儿茶素。它激活kelch样环氧氯丙烷相关蛋白1(Keap1)/核因子红细胞2相关因子2(Nrf2)信号通路以抑制氧化应激。Keap1/Nrf2信号通路不仅是多种抗氧化酶的上游信号靶点,还能使高水平的活性氧物质降至最低。本报告分析了EGCG在AD中的抗氧化作用,阐述了其具体作用机制,并为其在AD临床应用中提供了理论依据。

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