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氧化应激、神经炎症和 NADPH 氧化酶:在阿尔茨海默病发病机制和治疗中的意义。

Oxidative Stress, Neuroinflammation, and NADPH Oxidase: Implications in the Pathogenesis and Treatment of Alzheimer's Disease.

机构信息

Department of Biochemistry, MM Institute of Medical Sciences & Research, Maharishi Markandeshwar Deemed University, Mullana, Ambala, Haryana, India.

Department of Pharmacology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.

出版信息

Oxid Med Cell Longev. 2021 Apr 16;2021:7086512. doi: 10.1155/2021/7086512. eCollection 2021.

DOI:10.1155/2021/7086512
PMID:33953837
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8068554/
Abstract

NADPH oxidase as an important source of intracellular reactive oxygen species (ROS) has gained enormous importance over the years, and the detailed structures of all the isoenzymes of the NADPH oxidase family and their regulation have been well explored. The enzyme has been implicated in a variety of diseases including neurodegenerative diseases. The present brief review examines the body of evidence that links NADPH oxidase with the genesis and progression of Alzheimer's disease (AD). In short, evidence suggests that microglial activation and inflammatory response in the AD brain is associated with increased production of ROS by microglial NADPH oxidase. Along with other inflammatory mediators, ROS take part in neuronal degeneration and enhance the microglial activation process. The review also evaluates the current state of NADPH oxidase inhibitors as potential disease-modifying agents for AD.

摘要

NADPH 氧化酶作为细胞内活性氧(ROS)的重要来源,近年来受到了极大的重视,其家族所有同工酶的详细结构及其调节已经得到了很好的探索。该酶与多种疾病有关,包括神经退行性疾病。本综述简要回顾了 NADPH 氧化酶与阿尔茨海默病(AD)的发生和发展之间的联系。简而言之,有证据表明,AD 大脑中的小胶质细胞激活和炎症反应与小胶质细胞 NADPH 氧化酶产生的 ROS 增加有关。与其他炎症介质一起,ROS 参与神经元变性,并增强小胶质细胞激活过程。该综述还评估了 NADPH 氧化酶抑制剂作为 AD 潜在的疾病修饰剂的现状。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d08/8068554/05353a83aaf4/OMCL2021-7086512.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d08/8068554/05353a83aaf4/OMCL2021-7086512.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d08/8068554/05353a83aaf4/OMCL2021-7086512.001.jpg

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