Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá D.C., Colombia.
Nutr Neurosci. 2012 May;15(3):120-6. doi: 10.1179/1476830511Y.0000000033.
Parkinson's disease (PD) is a neurodegenerative movement disorder characterized by the degeneration and progressive loss of dopaminergic neurons in the substantia nigra pars compacta. It has been suggested that oxidative stress plays a role in the etiology and progression of PD. For instance, low levels of endogenous antioxidants, increased reactive species, augmented dopamine oxidation, and high iron levels have been found in brains from PD patients. In vitro and in vivo studies of Parkinson models evaluating natural and endogenous antioxidants such as polyphenols, coenzyme Q10, and vitamins A, C, and E have shown protective effects against oxidative-induced neuronal death. In this paper, we will review the mechanisms by which polyphenols and endogenous antioxidants can produce protection. Some of the mechanisms reviewed include: scavenging nitrogen and oxygen reactive species, regulation of signaling pathways associated with cell survival and inflammation, and inhibition of synphilin-1 and alpha-synuclein aggregation.
帕金森病（PD）是一种神经退行性运动障碍，其特征是黑质致密部多巴胺能神经元的退化和进行性丧失。有研究表明，氧化应激在 PD 的病因和进展中起作用。例如，在 PD 患者的大脑中发现了内源性抗氧化剂水平低、反应性物质增加、多巴胺氧化增强和铁水平升高。对评估天然和内源性抗氧化剂（如多酚、辅酶 Q10 和维生素 A、C 和 E）的帕金森模型的体外和体内研究表明，它们对氧化诱导的神经元死亡具有保护作用。在本文中，我们将综述多酚和内源性抗氧化剂产生保护作用的机制。综述的一些机制包括：清除氮和氧活性物质、调节与细胞存活和炎症相关的信号通路，以及抑制突触核蛋白-1 和α-突触核蛋白的聚集。
