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目的 探讨百草枯所致帕金森病 (Parkinson’sdisease ,PD)发病机制中是否有多巴胺D1受体和D2受体的参与。 方法 用口服百草枯的途径 ,建立小鼠慢性PD模型 ;应用免疫组织化学和原位杂交方法分别观察小鼠纹状体区多巴胺D1受体和D2受体蛋白和基因表达的情况。 结果 每天口服 10mg·kg-1百草枯的小鼠 ,4个月后自发性活动明显减少 ;纹状体区的多巴胺D1受体和D2受体蛋白含量较口服盐水对照组分别减少 2 8%和 2 9%(P <0 0 1) ,多巴胺D1受体和D2受体mRNA的表达较口服盐水对照组分别减少 2 9%和 33%(P <0 0 1)。 结论 百草枯可造成小鼠PD样的行为表现。纹状体区多巴胺D1受体和D2受体蛋白含量和基因表达的降低 ,提示了两种受体均参与了百草枯所致的PD发病机制。
Objective To investigate whether paraquat-induced dopamine D1 and D2 receptors are involved in the pathogenesis of Parkinson’s disease (PD). Methods The mouse model of chronic PD was established by oral administration of paraquat. The expression of dopamine D1 receptor and D2 receptor protein and gene in mouse striatum were detected by immunohistochemistry and in situ hybridization. Results After oral administration of 10 mg · kg -1 paraquat a day, the spontaneous activity decreased significantly after 4 months. The levels of dopamine D1 receptor and D2 receptor protein in the striatum were reduced by 28% and 40% respectively compared with the saline control group (P <0.01), and the expression of dopamine D1 receptor and D2 receptor mRNA decreased by 29% and 33% (P <0.01), respectively, compared with the saline control group. Conclusion Paraquat can cause PD-like behavior in mice. The striatal dopamine D1 receptor and D2 receptor protein content and gene expression decreased, suggesting that both receptors are involved in paraquat-induced PD pathogenesis.