Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei 430022, China.
Crit Rev Toxicol. 2012 Aug;42(7):613-32. doi: 10.3109/10408444.2012.680431. Epub 2012 May 11.
The etiology of Parkinson's disease (PD) is attributed to both environmental and genetic factors. The development of PD reportedly involves mitochondrial impairment, oxidative stress, α-synuclein aggregation, dysfunctional protein degradation, glutamate toxicity, calcium overloading, inflammation and loss of neurotrophic factors. Based on a link between mitochondrial dysfunction and pesticide exposure, many laboratories, including ours, have recently developed parkinsonian models by utilization of rotenone, a well-known mitochondrial complex I inhibitor. Rotenone models for PD appear to mimic most clinical features of idiopathic PD and recapitulate the slow and progressive loss of dopaminergic (DA) neurons and the Lewy body formation in the nigral-striatal system. Notably, potential human parkinsonian pathogenetic and pathophysiological mechanisms have been revealed through these models. In this review, we summarized various rotenone-based models for PD and discussed the implied etiology of and treatment for PD.
帕金森病（PD）的病因归因于环境和遗传因素。据报道，PD 的发展涉及线粒体损伤、氧化应激、α-突触核蛋白聚集、功能蛋白降解障碍、谷氨酸毒性、钙超载、炎症和神经营养因子缺失。基于线粒体功能障碍与农药暴露之间的联系，包括我们实验室在内的许多实验室最近利用鱼藤酮（一种众所周知的线粒体复合物 I 抑制剂）开发了帕金森病模型。PD 的鱼藤酮模型似乎模拟了特发性 PD 的大多数临床特征，并再现了黑质纹状体系统中多巴胺能（DA）神经元的缓慢进行性丧失和路易小体的形成。值得注意的是，通过这些模型揭示了潜在的人类帕金森病发病机制和病理生理学机制。在这篇综述中，我们总结了各种基于鱼藤酮的 PD 模型，并讨论了 PD 的发病机制和治疗方法。
