目的 研究龟板联合石菖蒲有效成分β-细辛醚对6-OHDA诱导的SD大鼠帕金森病（PD）模型的神经保护作用及机制。方法 以大鼠自主活动度和滚轴实验研究动物的行为学，以中脑黑质酪氨酸羟化酶（TH）观察多巴胺能神经元的损伤程度，并观察纹状体中α-突触核蛋白（α-syn）含量来探讨药物作用机制。结果 模型组自主活动次数、滚轴运动能力均显著低于正常对照组（P ＜0.05）；多巴胺能神经元中TH阳性细胞数明显减少；纹状体内的α-syn蛋白水平明显升高。龟板联合β-细辛醚给药后能明显改善模型组大鼠的行为学表现，增加TH阳性细胞数，降低纹状体内α-syn蛋白水平。结论 龟板联合β-细辛醚具有神经保护作用，能对抗模型组大鼠PD模型中的神经损伤，其机制可能与下调α-syn蛋白水平有关。

Objective To study the neuroprotective effect of combination of Carapax et Plastrum Testudinis and β-asarone against rat mode of Parkinson's disease（PD） induced by 6-hydroxydopamine（6-OHDA），and to explore its possible mechanism. Methods The behavioral changes were assessed by open field and rotarod test. The activities of tyrosine hydroxylase（TH） in substantia nigra of midbrain were examined by immunohistochemical staining for the evaluation of the damage of dopaminergic neurons. Moreover，the neuroprotective mechanism of the combination of Carapax et Plastrum Testudinis and β-asarone was investigated by the changes of α-synuclein level in the corpus striatum analyzed by ELISA. Results Compared with the blank control group，model rats had low autonomic activities and activites on rotating the rod（P ＜0.05）. The number of dopaminergic neurons with TH positive was reduced，and α-synuclein level in the corpus striatum was increased in the model group. After treatment with the combination of Carapax et Plastrum Testudinis and β-asarone，the behavior of PD rats was improved，TH-positive neurons count was increased，and α-synuclein level in the corpus striatum was decreased. Conclusion The combination of Carapax et Plastrum Testudinis and β-asarone damage has neuroprotective effect against neurogenic injury in 6-OHDA-induced PD rats，and the mechanism may be associated with the down-regulation of α-synuclein level.

R285.5

广东省自然科学基金（S2012010010625）；广州中医药大学第一临床医学院优秀博士学位论文培育项目（中医临-[2014]2号）。