中文摘要：

目的观察1-甲基-4-苯基-1，2，3，6-四氢吡啶（MPTP）致帕金森病（PD）模型小鼠黑质多巴胺能神经细胞过表达CalbindinD28k（CB）时，纹状体细胞抗损伤作用机制。方法选择C57BI，／6小鼠连续5d腹腔注射MPTP，构建成功PD模型小鼠30只，随机分为模型组，人类免疫缺陷病毒（HIV）-Ⅰ组（注射HIV-Ⅰ和CB-HIV-Ⅰ组（注射CB-HIV-Ⅰ），每组10只，连续6周对各组小鼠行为学检测，Westernblot法检测各组小鼠CB，Bcl-2和Ijax的表达变化。结果与模型组和HIV-Ⅰ组比较，CB—HIV-Ⅰ组小鼠各时间点移动格子次数，第1、2、5和6周站立次数，第6周时游泳和悬挂时间，差异有统计学意义（P〈0．05，P〈0．01）；CB-HIV-Ⅰ组小鼠中脑黑质中CB的表达量显著升高（P〈0．05），纹状体细胞中Bcl-2的表达量亦明显升高（P〈0．01），而Bax的表达量明显降低（P〈0．01）。模型组和HIVI组上述指标差异无统计学意义（P〉0．05）。结论黑质多巴胺能神经细胞过表达CB时，纹状体细胞Bcl-2／Bax表达上调，提示其与纹状体细胞抗凋亡能力增强有关。

英文摘要：

Objective To study the effect of over-expression of calbindin D28k（CB） in substantia nigra dopaminergic neurons on the expression of Bcl-2 and Bax in the striatum of 1-methyl-4-phe- nyl-1,2,3,6-tetrahydropyridine（MPTP）-induced mouse model of Parkinson＇s disease（PD） and to discover CB＇s neuroprotective mechanism at protein expression levels. Methods C57BL/6 mice were injected intraperitoneally with MPTP for 5 days to establish 30 mouse models of PD. Then, the mice were randomly divided into 3 groups（10 mice/group）：control group, HIV-Ⅰ group（in- jected with HIV-Ⅰ ）, and CB-HIV-Ⅰ group（injected with CB-HIV-Ⅰ ）. The Western blot was used to detect the expression levels of CB,Bcl-2 and Bax. Results Compared with control group and HIV-Ⅰ group,the expression of CB and bcl-2 increased （P 〈 0.05,P〈 0.01） ,while the ex- pression of bax decreased （P 〈 0.01） in CB-HIV-Ⅰ group. Conclusion The over-expression of CB in substantia nigra＇s dopaminergic neurons may promote striatum cells＇ resistance to apoptosis,which is related to the increase in Bcl-2/Bax ratio.