中文摘要：

探讨氧化应激参与帕金森病（PD）的发病机制。还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶 （NADPH oxidases,NOX）介导产生的活性氧参与帕金森病病理机制,笔者就还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶在帕金森病中的作用的研究历史进行了梳理,同时对血红素氧化酶-1在帕金森病中的神经保护作用及其与还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶的相互关系进行了综述,提出通过调控HO-1并可经还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶/活性氧通路能够在帕金森病中具有抗损伤作用,因此,筛选调控HO-1/NOX2轴有可能成为帕金森病治疗的新靶点。

英文摘要：

Accumulating evidence strongly supports the involvement of oxidative stress in the etiology of Parkinson＇s disease （PD）. ROS derived from the NOX2-containing NADPH oxidase play important role in the pathogenesis of PD. Our intent was to review the research history about the role of NOX2-containing NADPH oxidase in PD. Neuroprotective effect of heme oxygenase-1 （HO-1） in protecting neurons against PD-related neurotoxin-induced oxidative stress dependant injury, and a major emphasis has been on the relationship between HO-1 and NOX2-containing NADPH oxidase.Specific activation of HO-1 gene expression by pharmacological modulation may represent a novel target for therapeutic treatment of PD through inhibiting NOX/ROS. A new target for PD therapy through inhibiting NOX/ROS, thereby modulating HO-1/NOX2 axis is highlighted.