迷迭香酸对MPTP诱导的多巴胺神经元损伤的保护作用

摘要

Dopaminergic neurons injury is a key pathogenic factor at the onset of Parkinson's disease.To investigate the protective effect and possible mechanisms of rosemarinic acid (RA) on MPTP induced dopaminergic neurons injury,dopaminergic neurons were pretreated with rosemarinic acid for 30 min prior to MPTP treatment,neuron viability,ROS lever,caspase-3 lever and cleaved caspase-3 level were measured.Results showed that MPTP induced dopaminergic neuron viability decreased (P ＜ 0.05),ROS level and cleaved caspase-3 level increased (P ＜ 0.01).Moreover,the application of RA (40 iμmol/L and 20 μmol/L) can effectively reverse MPTP induced dopaminergic neuron viability decrease,ROS level and cleaved caspase-3 level increase (P ＜ 0.05,P ＜ 0.01).These results indicated that rosemarinic acid can protect MPTP induced dopaminergic neuron toxicity possibly through decreasing aberrant elevation of ROS and reverse abnormal aspase-3 activity.%多巴胺神经元损伤是PD发病的重要机制,本文利用1-甲基-4-苯基-1,2,3,6-四氢吡啶(1-methyl-4-pheyl-1,2,3,6-tetrahydrophridine,MPTP)诱导多巴胺神经元损伤,在诱导损伤前给予不同剂量迷迭香酸处理,采用细胞活性检测试剂盒(CCK-8)检测神经元的活性;活性氧(reactive oxygen species,ROS)检测试剂盒检测神经元ROS水平;Western blot(WB)检测神经元凋亡相关蛋白caspase-3和cleaved caspase-3的表达,研究迷迭香酸(Rosemarinic acid,RA)对MPTP诱导的神经元损伤的保护作用及可能机制.结果显示,MPTP处理可使多巴胺神经元活力显著降低(P＜0.05),ROS水平和cleaved caspase-3表达显著升高(P＜0.01);迷迭香酸预处理(40μmol/L和20μmol/L)可逆转MPTP诱导的多巴胺神经元活力降低,抑制MPTP诱导的多巴胺神经元ROS和cleaved caspase-3升高(P＜0.05,P＜0.01).迷迭香酸预处理对MPTP诱导的多巴胺神经元损伤具有保护作用,其机制可能与抑制ROS释放,阻止caspase-3异常激活有关.