咖啡因可预防百草枯和代森锰联合诱导的多巴胺能神经元变性。
Caffeine protects against combined paraquat and maneb-induced dopaminergic neuron degeneration.
机构信息
MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA.
出版信息
Exp Neurol. 2010 Jun;223(2):657-61. doi: 10.1016/j.expneurol.2010.02.007. Epub 2010 Feb 24.
Abstract
Environmental exposures suspected of contributing to the pathophysiology of Parkinson's disease (PD) include potentially neurotoxic pesticides, which have been linked to an increased risk of PD. Conversely, possible protective factors such as the adenosine antagonist caffeine have been linked to a reduced risk of the disease. Here we assessed whether caffeine alters dopaminergic neuron loss induced by exposure to environmentally relevant pesticides (paraquat and maneb) over 8weeks. The number of nigral neurons positive for tyrosine hydroxylase immunoreactivity (TH+) was assessed using stereological methods and found to be significantly reduced (to 60% of control) by combined pesticide treatment. Caffeine at 20mg/kg significantly reduced TH+ neuron loss (to 85% of the respective control). The results demonstrate the neuroprotective potential of caffeine in a chronic pesticide exposure model of model of PD.
摘要
环境暴露被怀疑导致帕金森病 (PD) 的病理生理学，包括潜在的神经毒性农药，这些农药与 PD 风险增加有关。相反，一些可能的保护因素，如腺苷拮抗剂咖啡因，与疾病风险降低有关。在这里，我们评估了咖啡因是否会改变暴露于环境相关农药（百草枯和代森锰锌） 8 周后诱导的多巴胺能神经元丢失。使用立体学方法评估酪氨酸羟化酶免疫反应性阳性（TH+）的黑质神经元数量，发现联合农药处理显著减少（至对照组的 60%）。咖啡因 20mg/kg 显著减少 TH+神经元丢失（至相应对照组的 85%）。结果表明，咖啡因在 PD 的慢性农药暴露模型中具有神经保护潜力。
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