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目的观察尼莫地平对帕金森病模型鼠多巴胺能神经元中Bcl-2、P53蛋白表达的影响,从而探索尼莫地平对黑质多巴胺能神经元的保护作用。方法建立大鼠PD模型,分组、分阶段用尼莫地平进行干预,第一阶段为尼莫地平对PD模型的预先干预,第二阶段为成功PD模型的药物治疗(尼莫地平、左旋多巴),其后均由阿朴吗啡(Apomorphine)诱导旋转行为,最后予大鼠黑质细胞进行HE、TH、Bcl-2、P53染色。结果第一阶段:尼莫地平PD模型组(Ⅰ组)和PD模型组(Ⅱ组),成功模型右侧黑质Bcl-2蛋白表达阳性细胞百分比较假手术组(Ⅲ组)和正常对照组(Ⅳ组)低(P<0.05),而P53蛋白表达阳性细胞百分比较Ⅲ组和Ⅳ组高(P<0.05);Ⅰ组右侧黑质Bcl-2蛋白表达阳性细胞百分比高于Ⅱ组(P<0.05),而P53蛋白表达阳性细胞百分比低于Ⅱ组(P<0.05);第二阶段:尼莫地平组、左旋多巴组或二者联用干预组与生理盐水组间右侧黑质Bcl-2、P53蛋白表达阳性细胞百分比无统计学差异(P>0.05)。结论尼莫地平在蛋白合成水平促进了Bcl-2表达、抑制了P53表达,减缓了多巴胺能神经元的凋亡。
Objective To observe the effect of nimodipine on the expression of Bcl-2 and P53 proteins in dopaminergic neurons in Parkinson’s disease rat model, and to explore the protective effect of nimodipine on dopaminergic neurons in substantia nigra. Methods The rat model of PD was established and divided into groups. Nimodipine was used to intervene in stages. The first phase was nimodipine’s intervention on PD model. The second phase was drug treatment of successful PD model (nimodipine, levodopa ), Followed by Apomorphine induced rotation, and finally to rat substantia nigra cells for HE, TH, Bcl-2, P53 staining. Results In the first phase, the percentages of Bcl-2 positive cells in substantia nigra on the right side of the nimodipine PD group (group Ⅰ) and PD model group (Ⅱ group) were significantly higher than those in sham operation group (Ⅲ) and normal control (P <0.05), while the percentage of P53 positive cells in group Ⅰ was higher than those in group Ⅲ and Ⅳ (P <0.05). The percentage of positive cells in group B was higher than that in group Ⅱ P <0.05), while the percentage of P53 positive cells was lower than that of group II (P <0.05). The second stage: the nimodipine group, levodopa group, There was no significant difference in the percentage of positive Bcl-2 and P53 protein expression (P> 0.05). Conclusion Nimodipine can promote the expression of Bcl-2 protein at the level of protein synthesis, inhibit the expression of P53 and slow down the apoptosis of dopaminergic neurons.