Gao Hui Ming, Liu Bin, Zhang Wangqin, Hong Jau Shyong
Neuropharmacology Section, Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences/National Institutes of Health, Research Triangle Park, NC 27709, USA.
Trends Pharmacol Sci. 2003 Aug;24(8):395-401. doi: 10.1016/S0165-6147(03)00176-7.
Parkinson's disease (PD) is a movement disorder that is characterized by progressive degeneration of the nigrostriatal dopamine system. Although dopamine replacement can alleviate symptoms of the disorder, there is no proven therapy to halt the underlying progressive degeneration of dopamine-containing neurons. Recently, increasing evidence from human and animal studies has suggested that neuroinflammation is an important contributor to the neuronal loss in PD. Moreover, the pro-inflammatory agent lipopolysaccharide itself can directly initiate degeneration of dopamine-containing neurons or combine with other environmental factor(s), such as the pesticide rotenone, to exacerbate such neurodegeneration. These effects provide strong support for the involvement of inflammation in the pathogenesis of PD. Furthermore, growing experimental evidence demonstrates that inhibition of the inflammatory response can, in part, prevent degeneration of nigrostriatal dopamine-containing neurons in several animal models of PD, suggesting that inhibition of inflammation might become a promising therapeutic intervention for PD.
帕金森病（PD）是一种运动障碍性疾病，其特征是黑质纹状体多巴胺系统进行性退化。尽管多巴胺替代疗法可以缓解该疾病的症状，但尚无经证实的疗法能够阻止含多巴胺神经元的潜在进行性退化。最近，来自人类和动物研究的越来越多的证据表明，神经炎症是帕金森病中神经元丢失的重要促成因素。此外，促炎剂脂多糖本身可直接引发含多巴胺神经元的退化，或与其他环境因素（如农药鱼藤酮）结合，加剧这种神经退化。这些效应为炎症参与帕金森病发病机制提供了有力支持。此外，越来越多的实验证据表明，在几种帕金森病动物模型中，抑制炎症反应可以部分预防黑质纹状体含多巴胺神经元的退化，这表明抑制炎症可能成为一种有前景的帕金森病治疗干预措施。
