【摘要】：帕金森病(Parkinson's disease,PD)是臨床常見的神經(jīng)退行性病變,病因與年齡、環(huán)境和遺傳等多方面因素密切相關(guān)。研究表明,PD多巴胺能神經(jīng)元變性壞死與氧化應(yīng)激條件下活性氧基團(reactive oxygen species,ROS)生成增多有關(guān),然而,Nrf2可調(diào)節(jié)細(xì)胞保護蛋白從而減少ROS生成,并通過其介導(dǎo)的抗氧化損傷通路,調(diào)控其上游和下游基因蛋白,參與抗氧化應(yīng)激反應(yīng)的修復(fù)過程。從Nrf2及其抗氧化損傷通路與PD相互作用和關(guān)系作一綜述,尋找其在抗氧化應(yīng)激方面的優(yōu)勢,為進一步探究PD的作用機制和治療方法提高可靠的依據(jù)。
[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.
【作者單位】： 解放軍醫(yī)學(xué)院;解放軍總醫(yī)院中醫(yī)院;
【基金】：國家自然科學(xué)基金項目(81273969) 北京市科技計劃“十病十藥”研發(fā)專項基金項目(Z131100002513015)
【分類號】：R742.5

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