Nrf2及其抗氧化损伤通路在帕金森病中的作用

发布时间：2018-11-21 09:25

【摘要】：帕金森病(Parkinson's disease,PD)是临床常见的神经退行性病变,病因与年龄、环境和遗传等多方面因素密切相关。研究表明,PD多巴胺能神经元变性坏死与氧化应激条件下活性氧基团(reactive oxygen species,ROS)生成增多有关,然而,Nrf2可调节细胞保护蛋白从而减少ROS生成,并通过其介导的抗氧化损伤通路,调控其上游和下游基因蛋白,参与抗氧化应激反应的修复过程。从Nrf2及其抗氧化损伤通路与PD相互作用和关系作一综述,寻找其在抗氧化应激方面的优势,为进一步探究PD的作用机制和治疗方法提高可靠的依据。
[Abstract]:Parkinson's disease (Parkinson's disease,PD) is a common neurodegenerative disease. Studies have shown that degeneration and necrosis of PD dopaminergic neurons are associated with increased production of reactive oxygen species (reactive oxygen species,ROS) under oxidative stress. However, Nrf2 can regulate cell protection proteins and thus reduce ROS production. The upstream and downstream gene proteins were regulated through the antioxidant injury pathway, which participated in the repair process of antioxidant stress response. This paper reviews the interaction and relationship between Nrf2 and its antioxidant injury pathway and PD, and looks for its advantages in antioxidant stress, which will provide a reliable basis for further exploring the mechanism and therapeutic methods of PD.
【作者单位】：解放军医学院;解放军总医院中医院;
【基金】：国家自然科学基金项目(81273969) 北京市科技计划“十病十药”研发专项基金项目(Z131100002513015)
【分类号】：R742.5

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