目的 建立1-甲基-4-苯基吡啶离子（1-methy1-4-phenyl pyridinium ion，MPP+）诱导的大鼠小脑颗粒细胞调亡横型。方法 MPP+处理大鼠小脑颗粒细胞。分别用甲基绿-派诺宁染色，DNA凝胶电泳。流式细胞术进行检测。结果 浓度为50 μrnol/L MPP+使小脑颗粒细胞发生调亡。结论以MPP+为诱导剂建立的大鼠小脑囊粒细胞调亡模型，可用于研究和帕金森病（PD）有关的细胞调亡的调控机制和筛选抗PD药物。

目的 观察类叶升麻苷对小鼠学习记忆能力的影响。方法 用东莨菪碱致小鼠记忆获得性障碍模型，以行为学实验（跳台法、水迷路法）、大脑皮层和纹状体乙酰胆碱酯酶活性和M受体的最大结合力为指标观察类叶升麻苷的作用。结果 在东莨菪碱致小鼠记忆障碍模型中，类叶升麻苷可延长跳台实验的平台停留期，并显著减少错误次数；在水迷路实验中可提高正确反应百分率；并能拮抗东莨菪碱所引起的大脑皮层乙酰胆碱酯酶的增高及皮层、纹状体M 受体最大结合力的降低。结论 类叶升麻苷对东莨菪碱所引起的小鼠学习记忆能力障碍有改善作用，其作用机制可能与抑制乙酰胆碱酯酶活性和激动M 受体的作用有关。

The neuroprotective effects of verbascoside, one of phenylpropanoid glucoside isolated from the Chinese herbal medicine Buddleja officinalis Maxim, on 1-methyl-4-phenylpyridinium ion (MPP+) induced apotosis and oxidative stress in PC12 neuronal cells were investigated. Treatment of PC12 cells with MPP+ for 48 h induced apoptotic death as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-dipheny ltetrazolium bromide (MTT) assay and flow cytometry, the activation of caspase-3 measured by the caspase-3 activity assay kit, the reduction in mitochondrial membrane potential with laser scanning confocal microscopy and the increase in the extracellular hydrogen peroxide level. Simultaneous treatment with verbascoside markedly attenuated MPP+ -induced apoptotic death, increased extracellular hydrogen peroxide level, the activation of caspase-3 and the collapse of mitochondrial membrane potential. These results strongly indicate that verbascoside may provide a useful therapeutic strategy for the treatment of oxidative stress-induced neurodegenerative disease such as Parkinson's disease.

In our study we investigated the neuroprotective effects of phenylethanoid glycosides (PhGs) from Cistanches salsa on 1-methyl-4-phenylpyridinium ion (MPP+)-induced apoptosis in cerebellar granule neurons (CGNs). CGNs were treated with 100 μM MPP+ for 24 h to induce apoptosis, simultaneously CGNs were incubated with PhGs at 10, 20 and 40 μg/ml, respectively. In addition CGNs were pretreated with PhGs at 20 μg/ml for 6, 12, 24 h, respectively, and then treated with 100 μM MPP+ for 24 h. 3-(4,5-Dimethylthiazol-2-ylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay revealed that the treatment of CGNs with PhGs inhibited the decrease of cell viability induced by MPP+. The activation of caspase-3 and caspase-8 was induced by MPP+ in apoptosis. The caspase-3 and caspase-8 fluorogenic assays showed that the treatments of CGNs with PhGs efficiently suppressed the activation of caspase-3 and caspase-8 induced by MPP+. It is concluded that PhGs can prevent the MPP+-induced apoptosis in CGNs and exert its anti-apoptosis effect by inhibiting caspase-3 and caspase-8 activities.