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目的:明确在C57BL/6小鼠纹状体过表达野生型的人源帕金森相关蛋白PINK1能否减轻由侧脑室注射鱼藤酮引起多巴胺神经元损伤。方法:通过向C57BL/6小鼠(雄性,7周龄,18～20g)左侧纹状体中注射带有GFP人源野生型PINK1及突变体PINK1G309D的慢病毒包装颗粒,两周后向小鼠左侧侧脑室中定位注射鱼藤酮,通过蛋白质印迹,免疫组化和行为学的方法检测PINK1对鱼藤酮引起多巴胺神经元损伤的影响。结果:蛋白质印迹和免疫组化的实验都证明了在C57BL/6小鼠纹状体过表达野生型的PINK1对于鱼藤酮引起多巴胺能神经元的减少有明显的抑制作用(P<0.01),但对鱼藤酮引起的行为学损伤没有明显的改善作用。
OBJECTIVE: To determine if PINK1, a wild-type wild-type human Parkinson’s protein, is involved in the striatum of C57BL / 6 mice to reduce the damage of dopamine neurons induced by injection of rotenone into the lateral ventricle. Methods: Lentiviral packaging particles with GFP human wild-type PINK1 and mutant PINK1G309D were injected into the left striatum of C57BL / 6 mice (male, 7 weeks, 18-20g) The left lateral ventricle was injected with rotenone, and the effect of PINK1 on rotenone-induced dopaminergic neuron injury was detected by Western blot, immunohistochemistry and behavioral methods. RESULTS: Both Western blot and immunohistochemistry experiments demonstrated that PINK1 overexpression in the striatum of C57BL / 6 mice significantly inhibited the decrease of dopaminergic neurons induced by rotenone (P <0.01) Rotenone induced behavioral injury did not significantly improve the role.