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目的:通过检测帕金森病(Parkinson’s disease,PD)MPTP模型小鼠海马内GFAP和p-CREB的表达,探讨PD认知障碍发生的原因。方法:雄性C57BL/6小鼠随机分为对照组和PD模型组,每组12只。PD模型组经腹腔注射MPTP和丙磺舒,3.5 d注射1次,共10次,持续5周,对照组小鼠注射等量生理盐水。在第6周,旷场试验和爬杆试验评价运动功能。免疫组化检测黑质、纹状体TH的表达及海马GFAP和p-CREB的表达;Western Blot检测p-CREB的表达。结果:旷场实验和爬杆实验结果显示PD模型组小鼠运动能力明显低于对照组(P<0.001)。免疫组化显示PD模型组黑质TH阳性神经元和纹状体TH阳性神经纤维均明显低于对照组(P<0.001),海马的GFAP阳性细胞的面积明显多于对照组。而Western Blot和免疫组化染色均显示PD模型组海马p-CREB的表达明显少于对照组(P<0.001)。结论:慢性PD模型小鼠海马内星形胶质细胞激活和p-CREB表达降低,可能参与了PD认知损害的病理过程。
OBJECTIVE: To investigate the causes of PD cognitive impairment by detecting the expression of GFAP and p-CREB in the hippocampus of mice with Parkinson’s disease (PD) MPTP. Methods: Male C57BL / 6 mice were randomly divided into control group and PD model group, with 12 rats in each group. PD model group were injected intraperitoneally MPTP and probenecid, 3.5 d injection 1 times a total of 10 times for 5 weeks, the control group of mice injected with normal saline. At week 6, open field test and climbing pole test evaluated motor function. Immunohistochemistry was used to detect the expression of substantia nigra and striatum TH and the expression of GFAP and p-CREB in hippocampus. The expression of p-CREB was detected by Western Blot. Results: The results of open field test and climbing pole test showed that the exercise ability of mice in PD model group was significantly lower than that in control group (P <0.001). Immunohistochemistry showed that TH positive neurons in substantia nigra and striatum TH positive nerve fibers in PD model group were significantly lower than those in control group (P <0.001). The area of GFAP positive cells in hippocampus was significantly more than that in control group. Western Blot and immunohistochemical staining showed that the expression of p-CREB in the hippocampus of PD model group was significantly less than that of the control group (P <0.001). Conclusion: Astrocyte activation and p-CREB expression in the hippocampus of chronic PD model mice are decreased, which may be involved in the pathological process of cognitive impairment of PD.