帕金森病氧化应激机制及抗氧化药物治疗进展

帕金森病(PD)是一种仅次于阿尔兹海默病的第二大神经系统变性疾病,随着社会人口老龄化,PD发病率逐年增高,在65岁以上的老年人,患病率高达1%。PD主要临床表现为静止性震颤、肌强直、运动迟缓、姿势步态异常。目前病因仍未明确,疾病发生与很多因素相关,其主要病理特征为黑质多巴胺能神经元变性缺失。研究发现线粒体功能障碍、钙超载、铁离子的堆积、免疫炎症等均与氧化应激有关,能造成氧化性损伤,促进多巴胺能神经元凋亡,氧化应激在促进PD疾病发展中起到重要作用,因而越来越备受关注,抗氧化治疗在某种程度上为PD的治疗指出新的方向。本文就氧化应激引起DA神经元变性缺失的机制及抗氧化药物的治疗进展进行综述。

The MechanismOxidative Stress and the Advanced Therapy of Antioxidant Agents in Parkinsion's Disease

Parkinsion''s disease is the second most common neurodegenerative disease after Alzheimer''s disease, the incidence of the disease has been increasing year by year, accompanied by aging in the society, it affects one in every 100 persons above the age of 65 years. The clinical manifestations include static tremor, myotonia, bradykinesia, abnormal gait and posture. The causes of disease have not been found, it is connected with many factors, but its main pathological feature is degeneration and absence of dopaminergic neurons in substantia nigra. Studies have found that dysfunction of mitochondria, calcium overload, ferrous iron accumulation, immunization inflammation all have connection with oxidative stress, which can lead to oxidative damage and promote dopaminergic neuron to apoptosis. oxidative stress plays an important role in the progress of PD, so under much attention, anti-oxidant therapy can provide a new approach for PD. This review pays attention to the mechanism of degeneration and absence of dopaminergic neurons that be caused by oxidative stress and advanced therapy of Antioxidant agents.