帕金森病氧化应激机制的研究进展

The research progress of oxidative stress mechanism of Parkinson's disease

帕金森病(parkinson's disease,PD)是一种发病率随年龄增长而增加的中枢神经系统退行性疾病,患者大多为65岁以上的老年人。PD最主要的病理特征是中脑黑质致密区多巴胺能神经元发生变性坏死,导致黑质纹状体通路多巴胺(dopamine,DA)神经递质生成减少,从而造成患者出现运动迟缓、肌强直、静止性震颤、姿势平衡障碍等一系列症状。帕金森病的具体发病机制尚不明确,其与氧化应激、神经炎症、遗传、环境等很多因素有关。氧化应激在促进PD的发生发展中起到重要作用,引起越来越多学者的重视。抗氧化治疗在一定程度上为PD的治疗开辟了新的方向。研究发现线粒体功能障碍、多巴胺的代谢、金属离子含量异常等均与氧化应激有关,能对DA能神经元造成氧化性损伤,促进其凋亡。本文就氧化应激引起DA能神经元变性缺失的机制及其抗氧化治疗进行综述。

Parkinson's disease(PD)is a degenerative disease of the central nervous system that increases with age.Most of the patients are over 65 years old.The most major pathological feature of PD is that dopaminergic neurons in the substantia nigra pars compacta are degeneration and necrosis,leading to a decreased dopamine(DA)level in the substantia nigra striatum pathway,and resulting in a series of symptoms such as bradykinesia,myotonia,quiescent tremor and postural balance disorder.The specific pathogenesis of Parkinson's disease is not clear,which is related to oxidative stress,neuroinflammation,genetics,environment and many other factors.Oxidative stress plays an important role in promoting the occurrence and development of PD,which attract more attention to it.Antioxidant therapy opens up a new direction for the treatment of PD to some extent.Studies have found that mitochondrial dysfunction,dopamine metabolism and abnormal metal ion content are all related to oxidative stress,which can cause oxidative damage to DA neurons and promote their apoptosis.In this paper,the mechanism of denaturation of DA neurons caused by oxidative stress and its antioxidant treatment are reviewed.