血红素加氧酶1在阿尔茨海默病中的神经保护作用研究进展

Research Progress of the Neuroprotective Effect of Heme Oxygenase-1 in Alzheimer Disease

氧化应激是阿尔茨海默病(AD)的一个显著病理特征。AD中存在氧化应激,在生物化学和神经病理水平,在受累脑区脂质、核酸和蛋白氧化损伤的标志物存在于退变的神经元之中。鉴于氧化应激对神经病理形成的影响,针对抗氧化损伤成为治疗AD的重要方法。研究表明,受核转录因子Nrf2调节的血红素加氧酶1(HO-1)参与细胞抗氧化损伤,进而成为了AD中神经保护的新靶标。该文将就HO-1在AD中作用和相关机制予以综述。

A large body of evidence indicates that oxidative stress is a salient pathological feature in Alzheimer disease（AD）.In addition to signs of systemic oxidative stress,at the biochemical and neuropathological level,neuronal degeneration in these disorders has been shown to coincide with several markers of oxidative damage to lipids,nucleic acids,and proteins in affected brain regions.Given the pathogenic impact of oxidative stress,therapeutic strategies aimed to blunt these processes are considered an effective way to confer neuroprotection.Recently,the nuclear transcription factor Nr2-induced heme oxygenase-1 （HO-1）expression has been reported to have neuroprotective function against oxidative shsss（OS）,providing a new therapeutic target for AD.Here is to make a review of the role of H-1 in AD and its mechanisms.