MPTP诱导的帕金森病鼠脑内Calbindin-D28k表达的免疫组化研究

IMMUNOHISTOCHEMICAL STUDY OF CALBINDIN-D28K EXPRESSION IN THE BRAIN OF PARKINSONIAN MICE INDUCED BY MPTP

目的探讨Calbindin-D28k在帕金森病发病过程中的作用。方法健康C57BL/6J小鼠采用MPTP腹腔注射建立帕金森病动物模型,动物存活期分别为14d和28d。应用ABC免疫组化结合图像分析技术观察Calbindin-D28k在不同脑区的表达。结果帕金森病鼠脑内黑质和腹侧被盖区Calbindin-D28k的表达在28d比对照组增加,造模后海马CA1区Calbindin-D28k的表达在14d和28d两个时间点均比对照组增加;而在脑皮质Calbindin-D28k的表达在造模14d和28d均较对照组降低。结论不同脑区神经元可能由于Calbindin-D28k含量的不同而对MPTP的敏感性不同;帕金森病鼠不同脑区Calbindin-D28k表达的变化,可能是脑内神经元启动自我保护机制引起Calbindin-D28k在不同脑区重新分配,以达到保护损伤神经元的目的。

Objective To investigate the role of ealbindin-D28k in Parkinson＇s disease. Methods C57 BL/6J mice were injected intraperitoneally with MPTP to induce the Parkinsonian model. The animals were killed respectively on the 14th and the 28th day after injection. ABC immunohistochemistry and image analytical techniques were used. Results The expression of calbindin-D28k was increased in substantia nigra （SN） and ventral tegmental area of Tasi （VTA） on the 28th day and in CA1 of the hippocampus on 14th and 28th day, while the expression in the cerebral cortex was decreased after modeling. Conclusion The results suggest that the vulnerability of neurons to MPTP is different in the different cerebral areas with different calbindin-D28k contents in neurons. The changes in the expression of calbindin-D28k in after MPTP treatment might be related to the neuron self-protection. Calbindin- D28k rearrangement in the brain might protect the injured neurons.