中文摘要：

为探讨ATP敏感性钾通道（KATP）亚基Kit6．1、Kit6．2在帕金森病（PD）病理生理机制中的可能作用。本研究采用蛋白免疫印迹分析（Westernblot）对1-甲基4-苯基-1，2，3，6-四氢吡啶（MPTP）诱导的PD小鼠模型黑质、纹状体Kit6．1、Kit6．2在不同时间点表达变化进行检测，并与酪氨酸羟化酶（TH）的变化进行比较。结果发现：（1）与正常对照组相比，黑质、纹状体TH蛋白的表达在给药后第1d即开始下降，且呈时间依赖性下降（P〈0．01）；（2）黑质Kit6．1蛋白的表达在给药后第5d才开始下降（P〈0．01）；而纹状体Kit6．1蛋白的表达在给药后第5d才开始升高（P〈0．01）；（3）黑质Kit6．2蛋白的表达在给药后第5d才开始明显升高（P〈0．01）；而纹状体Kit6．2蛋白的表达在给药后第3d轻度升高（P〈0．05），第5d又明显降低（P〈0．01）。以上结果提示作为KATP通道亚基的Kit6．1、Kit6．2在MPTP的作用下，可能通过参与星形胶质细胞的活化、胆碱能突触传递的抑制以及自身代偿和修复在PD的病理生理过程中发挥了重要的角色。

英文摘要：

To investigate the roles of Kit6, 1 and Kit6.2 subunits in the pathological mechanism of Parkinson＇s disease （PD）. Western blot was used to detect the alterations of Kit6 proteins in different time courses （0, 1,3 and 5 days after 1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine （MPTP） injections） at different structures of brain （ the striatum and substantia nigra） in parkinsonian mice. The alterations of the Kit6 proteins were also compared with those of tyrosine hydroxylase （TH）. The results demonstrated that （ 1 ） the expression of TH protein was declined in a dose-dependent manner （ P 〈 0.01 ） one day after MPTP treatment ; （2） the expression of Kit6.1 protein was decreased in the substantia nigra but increased in the striatum at day 5 after MPTP treatment （ P 〈 0.01 ） ; （ 3 ） the expression of Kit6.2 protein began to increase in the substantia nigra at day 5 after MPTP infusion （ P 〈0.01 ）, starting to enhance in the striatum at day 3 after MPTP administration （ P 〈 0.05 ）, while beginning to decline at day 5 following MPTP insult （ P 〈 0.01 ）. It is concluded that the alterations of Kit6 proteins are delayed compared with the TH in MPTP-intoxicated mice, and MPTP oppositely alters the expression of Kit6 protein. Kit6 subunits are involved in the pathophysiology of PD via activating the astrocytes, inhibiting the cholinergic making self-reparation.