Joint International Research Laboratory of Ethnomedicine of Ministry of Education and Key Laboratory of Basic Pharmacology of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, China.
Oxid Med Cell Longev. 2020 Jul 3;2020:6137521. doi: 10.1155/2020/6137521. eCollection 2020.
Parkinson's disease (PD) is a chronic and complex disease of the central nervous system (CNS). Progressive loss of dopamine (DA) neurons in midbrain substantia nigra is considered to be the main cause of PD. The hallmark of PD pathology is the formation of Lewy bodies and the deposition of -synuclein (-syn). The mechanisms responsible for the progressive feature of DA neurodegeneration are not fully illustrated. Recently, oxidative stress and neuroinflammation have received extensive attention as two important entry points in the pathogenesis of PD. The occurrence of oxidative stress and neuroinflammation is usually derived from external influences or changes in internal environment, such as the accumulation of reactive oxygen species, exposure to a toxic environment, and the transformation of systemic inflammation. However, PD never results from a single independent factor and the simultaneous participation of oxidative stress and neuroinflammation contributed to PD development. Oxidative stress and neuroinflammation could potentiate each other to promote progression of PD. In this review, we briefly summarized the conditions of oxidative stress and neuroinflammation and the crosstalk between oxidative stress and neuroinflammation on the development of PD.
帕金森病（PD）是一种慢性且复杂的中枢神经系统（CNS）疾病。中脑黑质多巴胺（DA）神经元的进行性丧失被认为是 PD 的主要原因。PD 病理学的标志是路易体的形成和 -突触核蛋白（-syn）的沉积。导致 DA 神经退行性变进行性特征的机制尚未完全阐明。最近，氧化应激和神经炎症作为 PD 发病机制的两个重要切入点受到广泛关注。氧化应激和神经炎症的发生通常源于外部影响或内部环境的变化，例如活性氧物质的积累、暴露于有毒环境以及全身炎症的转化。然而，PD 从未由单个独立因素引起，氧化应激和神经炎症的同时参与促进了 PD 的发展。氧化应激和神经炎症可以相互增强，从而促进 PD 的进展。在这篇综述中，我们简要总结了氧化应激和神经炎症的情况，以及氧化应激和神经炎症在 PD 发展过程中的相互作用。
