帕金森病MPTP食蟹猴模型嗅球细胞凋亡

目的 建立1-甲基-4-苯基-1, 2, 3, 6-四氢吡啶（MPTP）帕金森病（PD）模型，探讨模型组嗅球细胞凋亡和胶质细胞增生情况。方法 3只成年健康食蟹猴，静脉注射MPTP建立PD模型，另3只静脉注射生理盐水作为对照。取出嗅球，免疫组织化学染色检测Caspase-3、Bcl-2、离子钙接头蛋白分子1（Iba-1）和胶质纤维酸性蛋白（GFAP）在食蟹猴嗅球中的表达情况，采用Image J v1.8.0软件分析模型组和对照组之间的差异。 结果 MPTP损伤后，与对照组相比，模型组嗅球突触小球层Caspase-3阳性细胞数明显增加，而Bcl-2表达减少；与对照组相比，模型组嗅球突触小球层和外网状层的GFAP和Iba-1阳性细胞数增加。 结论 MPTP可诱导食蟹猴嗅球突触小球层细胞凋亡，并伴有星形胶质细胞增生和小胶质细胞激活，这可能与帕金森病的功能障碍有关。

Apoptosis of olfactory bulb cells in MPTP cynomolgus monkey model of Parkinson’s dise

Objective To explore the apoptosis and the proliferation of glia cells in olfactory bulb of cynomolgus monkeys damaged by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Methods Three adult cynomolgus monkeys were injected with MPTP to induce the damage of olfactory bulb as MPTP group (model group) and other three adult cynomolgus monkeys as saline group (control group). Immunohistochemical staining was performed to examine the expression of Caspase-3, Bcl-2, ionized calcium binding adaptor molecule-1(Iba-1) and glial fibrillary acidic protein(GFAP) in the olfactory bulb. The numbers of Caspase-3, Bcl-2, Iba 1 and GFAP-positive cells were counted and the average absorbance was measured by Image J v1.8.0 in control and MPTP group. Results Compared with the normal control group, Caspase-3-positive cells increased significantly in the glomerular layer (GL) of olfactory bulb, and Bcl-2-positive cells decreased significantly in MPTP group after MPTP injury, and GFAP-positive and Iba-1-positive cells were located in GL and external plexiform layers (EPL). The number of GFAP-positive and Iba-1-positive cells increased in olfactory bulb in the MPTP group. Conclusion MPTP can induce the cell apoptosis, astrocyte and microglial activation in olfactory bulb of cynomolgus monkeys, which may be associated with the dysosmia in Parkinson’s disease.