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目的 :探讨囊泡单胺转运体 2 (vesicularmonoaminetransporter 2 ,VMAT2 )是否参与百草枯所致帕金森病 (Parkinson’sdisease ,PD)的发病机制。方法 :用口服百草枯的途径 ,建立小鼠PD模型 ;应用免疫组织化学和原位杂交法分别观察小鼠纹状体区VMAT2的水平和黑质部基因表达的变化。结果 :每天口服百草枯 10mg·kg-1的C5 7BL/ 6小鼠 ,2个月后自发性活动明显减少。纹状体区的VMAT2含量较口服盐水对照组减少 5 1 7% (P <0 0 1) ,黑质部VMAT2mRNA的表达降低 5 2 7% (P <0 0 1)。结论 :百草枯可造成小鼠PD样的行为表现 :黑质纹状体通路VMAT2含量和基因表达的降低 ,提示VMAT2参与了百草枯所致的PD发病机制。
OBJECTIVE: To investigate whether vesicular monoamine transporter 2 (VMAT2) participates in the pathogenesis of Parkinson’s disease (PD) induced by paraquat. Methods: Mouse model of PD was established by oral administration of paraquat. The level of VMAT2 and the gene expression of substantia nigra were detected by immunohistochemistry and in situ hybridization. Results: C5 7BL / 6 mice orally administered paraquat 10 mg · kg-1 at 2 months had a significant reduction in spontaneous activity. The VMAT2 content in the striatum decreased by 51.7% (P <0.01) compared with the saline control group, and the VMAT2 mRNA expression in the substantia nigra was reduced by 52.7% (P <0.01). CONCLUSION: Paraquat causes PD-like behavior in mice: decreased VMAT2 content and gene expression in the nigrostriatal pathway suggest that VMAT2 is involved in the pathogenesis of paraquat-induced PD.