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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 protective effect of protocatechuic acid on dopaminergic neuron damage in mouse embryonic midbrain after intervention with 1-methyl-4-phenylpyridinium ion (MPP +). METHODS: Cultured embryonic midbrain neurons of 14-day-old pregnant mice were cultured and cultured continuously for 7 days. The Parkinson’s disease (PD) model was induced by dopaminergic neurons in the midbrain of MPP + mice in vitro. The experiment was divided into control group, model group , Protoporphyrin (0.05 mmol / L), medium (0.1 mmol / L) and high (0.5 mmol / L). The viability of neurons was measured by MTT colorimetric assay. The content of lactate dehydrogenase (LDH) and reactive oxygen species (ROS) in the cells was determined. The mitochondrial complex I activity and membrane potential were measured. Results Protocatechuic acid increased the activity of dopaminergic neurons in MPP + -induced mesencephalon, reduced the release of LDH, reduced the production of ROS, decreased the activity of mitochondrial complex I and prevented the mitochondrial membrane potential from decreasing. Conclusion Protocatechuic acid has a protective effect on MPP + -induced mesencephalic dopaminergic neuron injury.