IL-17A敲除对帕金森病模型小鼠神经退变及神经炎症的影响

Effect of IL-17A knockout on neurodegeneration and neuroinflammation in a mouse model of Parkinson′s disease

目的:研究白细胞介素(interleukin)-17A对帕金森病(Parkinson′s disease,PD)模型鼠神经退变及神经炎症的影响。方法:IL-17A基因敲除的C57BL/6雄性小鼠通过腹腔注射1-甲基-4-苯基-1,2,3,6-四氢吡啶(1-methy-4-phenyl-1,2,3,6-tetrahydropyridine,MPTP)制备PD模型,注射的第7天取小鼠全脑,用TUNEL试剂盒检测中脑黑质部细胞的凋亡,用免疫组织化学法和Western Blot法检测黑质部小胶质细胞CD11b的表达。结果:IL-17A-/-的PD模型小鼠黑质部位细胞凋亡的数目较野生型PD模型小鼠减少,小胶质细胞的形态改变较轻且CD11b蛋白表达减少。结论:IL-17A基因敲除后减轻了PD模型小鼠的神经退变和神经炎症的变化。

Objective: To explore the effects of interleukin(IL)-17 A on mouse model of Parkinson′s disease(PD). Methods: 1-methy-4-phenyl-1, 2, 3, 6-tetrahydropyridine(MPTP) was intraperitoneally injected into the male and C57 BL/6 mice knocked out of IL-17 A gene to prepare PD model. The brain of mice was taken on day 7 after MPTP injection. The apoptosis of substantia nigra cells were detected by TUNEL kit, and the expression of CD11 b in the microglia of the substantia nigra was detected by Immunohistochemistry and Western Blot. Results: The number of apoptosis in the substantia nigra of mice with PD model mice of IL-17 A-/-was lower than the wild-type PD model mice, and the morphology of microglia was not obviously changed, and the expression of CD11 b protein is reduced. Conclusion: IL-17 A gene knockout reduces the changes in neurodegeneration and neuroinflammation in PD model mice.