目的 探讨原儿茶酸对1-甲基-4-苯基吡啶离子（MPP⁺）干预后的小鼠胚胎中脑多巴胺能神经元损伤的保护作用。方法 分离培养孕14 d小鼠胚胎中脑神经元细胞，连续培养7 d，以MPP⁺体外损伤小鼠胚胎中脑多巴胺能神经元诱导帕金森病（PD）模型，实验分为对照组，模型组，原儿茶酸低（0.05 mmol/L）、中（0.1 mmol/L）、高（0.5 mmol/L）剂量组。采用MTT比色法测定神经元活力，测定细胞内乳酸脱氢酶（LDH）、活性氧物质（ROS）的量，检测线粒体复合物I活性及膜电位。结果 原儿茶酸可增强MPP⁺损伤的中脑多巴胺能神经元活力，减少LDH释放，降低ROS产生，抑制线粒体复合物I活力下降，阻止线粒体膜电位降低。结论 原儿茶酸对MPP⁺诱导的中脑多巴胺能神经元损伤具有保护作用。

Objective To investigate the effects of protocatechuic acid (PCA) on the midbrain dopaminergic neurons injured by 1-methyl-4-phenylpyridinium (MPP⁺). Methods Midbrain neuron cells from KM mice pregnant 14 d were used in this experiment, and divided into control group, model group, low-, mid-, and high-dose (0.05, 0.1, and 0.5 mmol/L) groups. MTT method was used to determine the neuronal survival rate. The activity of lactate dehydrogenase (LDH) in culture, content of intracellular reactive oxygen species (ROS), activity of mitochondrial complex I, and mitochondrial membrane potential were further determined. Results PCA can enhance the viability of dopaminergic neurons damaged by MPP⁺, reduce the release of LDH and the generation of ROS, increase the activity of the mitochondrial complex Ι, and prevent the reduction of mitochondrial membrane potential. Conclusion PCA has the neroprotective effects against MPP⁺-induced damage of midbrain dopaminergic neurons.

国家自然科学基金资助项目（81102828，81273037）；山东省自然科学基金资助项目（2015ZRB14548）