文献类型：期刊文献

英文题名：Epigallocatechin-3-Gallate Inhibits Oxidative Stress Through the Keap1/Nrf2 Signaling Pathway to Improve Alzheimer Disease

作者：Tang, Shi[1];Zhang, Yong[1];Botchway, Benson O. A.[2,3];Wang, Xichen[1];Huang, Min[1];Liu, Xuehong[1]

机构：[1]Shaoxing Univ, Sch Med, Dept Histol & Embryol, Shaoxing 312000, Peoples R China;[2]Bupa Cromwell Hosp, London, England;[3]Univ Nicosia, Med Sch, Dept Basic & Clin Sci, Nicosia, Cyprus

年份：2024

外文期刊名：MOLECULAR NEUROBIOLOGY

收录：SCI-EXPANDED(收录号：WOS:001316798400001)、、Scopus(收录号：2-s2.0-85204287098)、WOS

语种：英文

外文关键词：Alzheimer disease; Oxidative stress; Epigallocatechin-3-gallate; Keap1/Nrf2 signal pathway; Degenerative disease; Antioxidant; Polyphenol

外文摘要：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.