Neurodegenerative diseases share various pathological features, such as accumulation of aberrant protein aggregates, microglial activation, and mitochondrial dysfunction. These pathological processes are associated with generation of reactive oxygen species (ROS), which cause oxidative stress and subsequent damage to essential molecules, such as lipids, proteins, and DNA. Hence, enhanced ROS production and oxidative injury play a cardinal role in the onset and progression of neurodegenerative disorders. To maintain a proper redox balance, the central nervous system is endowed with an antioxidant defense mechanism consisting of endogenous antioxidant enzymes. Expression of most antioxidant enzymes is tightly controlled by the antioxidant response element (ARE) and is activated by nuclear factor E2-related factor 2 (Nrf2). In past years reports have highlighted the protective effects of Nrf2 activation in reducing oxidative stress in both in vitro and in vivo models of neurodegenerative disorders. Here we provide an overview of the involvement of ROS-induced oxidative damage in Alzheimer's disease, Parkinson's disease, and Huntington's disease and we discuss the potential therapeutic effects of antioxidant enzymes and compounds that activate the Nrf2-ARE pathway.

译文

神经退行性疾病具有多种病理特征,例如异常蛋白聚集体的积累,小胶质细胞激活和线粒体功能障碍。这些病理过程与活性氧 (ROS) 的产生有关,活性氧 (ROS) 会导致氧化应激并随后对必需分子 (例如脂质,蛋白质和DNA) 造成损害。因此,增强的ROS产生和氧化损伤在神经退行性疾病的发生和发展中起主要作用。为了保持适当的氧化还原平衡,中枢神经系统具有由内源性抗氧化酶组成的抗氧化防御机制。大多数抗氧化酶的表达由抗氧化反应元件 (ARE) 严格控制,并由核因子E2-related因子2 (Nrf2) 激活。在过去的几年中,报告强调了Nrf2激活在减少神经退行性疾病的体外和体内模型中的氧化应激中的保护作用。在这里,我们概述了ROS诱导的氧化损伤在阿尔茨海默氏病,帕金森氏病和亨廷顿氏病中的作用,并讨论了激活Nrf2-ARE途径的抗氧化酶和化合物的潜在治疗作用。

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