Department of Pharmaceutical Chemistry and Drug Analysis, Research Group Experimental Neuropharmacology, Vrije Universiteit Brussel, Laarbeeklaan 103, 1090 Brussels, Belgium.
J Renin Angiotensin Aldosterone Syst. 2010 Mar;11(1):49-56. doi: 10.1177/1470320309347789. Epub 2009 Oct 27.
Since the discovery of a renin-angiotensin system (RAS) in the brain, several studies have linked this central RAS to neurological disorders such as ischaemia, Alzheimer's disease and depression. In the last decade, evidence has accumulated that the central RAS might also play a role in Parkinson's disease. Although the exact cause of this progressive neurodegenerative disorder of the basal ganglia remains unidentified, inflammation and oxidative stress have been suggested to be key factors in the pathogenesis and the progression of the disease. Since angiotensin II is a pro-inflammatory compound that can induce the production of reactive oxygen species due to activation of the NADPH-dependent oxidase complex, this peptide might contribute to dopaminergic cell death. In this review, three different strategies to interfere with the pathogenesis or the progression of Parkinson's disease are discussed. They include inhibition of the angiotensin-converting enzyme, blockade of the angiotensin II type 1 receptor and stimulation of the angiotensin II type 2 receptor.
自发现脑内肾素-血管紧张素系统（RAS）以来，已有多项研究将该中枢 RAS 与缺血性疾病、阿尔茨海默病和抑郁症等神经系统疾病联系起来。在过去的十年中，有证据表明中枢 RAS 也可能在帕金森病中发挥作用。尽管基底神经节这种进行性神经退行性疾病的确切病因仍未确定，但炎症和氧化应激被认为是发病机制和疾病进展的关键因素。由于血管紧张素 II 是一种促炎化合物，可通过激活 NADPH 依赖性氧化酶复合物诱导活性氧的产生，因此该肽可能导致多巴胺能神经元死亡。在这篇综述中，讨论了三种不同的干预帕金森病发病机制或进展的策略。它们包括抑制血管紧张素转换酶、阻断血管紧张素 II 型 1 受体和刺激血管紧张素 II 型 2 受体。
