肌苷对帕金森病小鼠模型的神经保护作用

目的: 观察肌苷对MPTP致帕金森病(PD)小鼠模型的神经保护作用.方法: 用MPTP建立C57BL小鼠PD模型,在MPTP前给予肌苷,通过行为学检测(自主活动计数、Rotarod检测、游泳实验)、免疫组织化学和荧光分光光度法,观察肌苷对PD小鼠模型的行为学表现、黑质多巴胺(DA)神经元和纹状体酪氨酸羟化酶免疫反应阳性(TH-ir)神经纤维以及纹状体DA水平的影响.结果: 给予MPTP后,小鼠行为学计数降低,自主活动计数、Rotarod检测、游泳实验分别降低约45%、43%和22%,黑质DA神经元数目减少约58%,纹状体TH-ir神经纤维密度减低,纹状体DA水平明显降低约88%,提前给予肌苷后降低程度减轻,自主活动计数、Rotarod检测、游泳实验降低程度分别约为5%、11%和12%,黑质DA神经元数目减少约43%,纹状体DA水平降低约71%,两组相比有显著性差异(P＜0.01).结论: 肌苷对MPTP所致的C57BL小鼠的神经损伤具有保护作用.

Inosine is neuroprective against MPTP-induced Parkinson's disease in C57BL mice

AIM: To study the neuroprotective effects of inosine on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced Parkinson's disease(PD) in C57BL mice. METHODS: The PD models were formed with intraperitoneal injections of MPTP. Inosine was administered intraperitoneally to mice 30 min prior to MPTP. The effects of inosine and MPTP on the behavioral exhibition, the number of dopamine (DA) neurons in the substantia nigra and the density of tyrosine hydroxylase-immunoreactive (TH-ir) nerve fibers in the striatum, and the level of DA in the striatum were studied by behavioral test, immunohistochemical analysis and fluorospectrophotometry. RESULTS: The scores of locomotion, Rotarod and swim test decreased by about 45% and 43% and 22%, respectively. The number of DA neurons in the substantia nigra declined by about 58%, the density of TH-ir nerve fibers also decreased, and the level of DA in the striatum declined by about 88%. Inosine, given prior to MPTP, attenuated the effects of MPTP. The scores of locomotion, Rotarod and swim test declined only by about 5% and 11% and 12%, respectively, the number of DA neurons in the substantia nigra declined by only about 43% and the level of DA in the striatum declined only by about 71%. CONCLUSION: Inosine is neuroprective against MPTP-induced lesions in C57BL mice.