目的:研究内质网应激反应在1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)所致帕金森病(PD)小鼠模型黑质区多巴胺能神经元凋亡的作用.方法:将小鼠随机分为MPTP模型组、Rb1干预剂组和对照组.观察行为学,免疫组织化学和免疫蛋白印迹法观察黑质酪氨酸羟化酶(TH)、葡萄糖调节蛋白78 (GRP78)、半胱氨酸蛋白酶-12 (caspase-12)和半胱氨酸蛋白酶-3 (caspase-3)的表达.结果:与对照组相比,模型组小鼠出现典型PD症状,TH阳性神经元明显丢失、蛋白水平下降,GRP78、caspase-12、caspase-3阳性细胞及蛋白水平增加;经人参皂甙Rb1处理后,上述变化均减轻.结论:内质网应激(ERS)在MPTP诱导的PD小鼠模型多巴胺能神经元凋亡中可起重要作用,人参皂甙Rb1可通过抑制ERS而对PD小鼠具有一定的神经保护作用.%Objective: To explore the role of endoplasmic reticulum stress (ERS) in apoptosis of dopaminergic neurons in substantia nigra (SN) of MPTP-induced Parkinson's disease mouse model, therefore, to validate whether ginsenoside Rbl alleviate the apoptosis above-mentioned. Methods: Healthy male C57BL/6N mice were randomly divided into 3 groups: MPTP model group, Rbl group and control group. Besides of behavior, the number of positive cell for tyrosine hydroxylase (TH), glucose-regulated protein (GRP78), caspase-12 and caspase-3 and the expression levels of these proteins in the SN of midbrain were detected using immunohistochemistry and Western blot. Results: Compared with control mice, the model animals showed typical symtoms of PD with decreased positive cell number and expression level of TH, and markedly increased positive cell number and expression levels of GRP78, caspase-12 and caspase-3 in SN of the midbrain. After giving Rbl, the above changes were alleviated obviously. Conclusion: In MPTP-induced PD mouse model, ERS mediates the SN dopaminergic neurons to apoptosis that can be suppressed by ginsenoside Rb1.
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