中文摘要：

目的探讨1,5-二咖啡酰奎宁酸（1,5-dicaffeoylquinic acid,1,5-diCQA）对多巴胺能神经元的保护作用及其可能的机制。方法采用1-甲基-4-苯基吡啶离子（MPP^＋）诱导具有多巴胺能神经元特性的PC12细胞作为帕金森病的体外模型,实验分为正常对照组、MPP^＋组和1,5-diCQA预处理组,根据1,5-diCQA预处理的浓度,将后者又分为10、20、50、100μmol/L 4组。用MTT法测定各组细胞存活率,酶标仪检测细胞活性氧簇（reactive oxygen species,ROS）含量和谷胱甘肽（glutathione,GSH）水平,RT-PCR法检测细胞突触核蛋白（α-synuclein）的mRNA表达水平,Western blot检测各组细胞α-synuclein蛋白表达水平。结果 MPP^＋（250μmol/L）处理PC12细胞24 h后,与正常对照组相比,细胞存活率下降,ROS生成增多,GSH耗竭;不同浓度的1,5-diCQA预处理可以减轻MPP^＋导致的细胞损伤,且在一定范围内具有量-效关系;50μmol/L的1,5-diCQA预处理可以显著抑制MPP^＋诱导的α-synuclein转录和翻译水平的增加。结论 1,5-diCQA对MPP^＋诱导的PC12细胞氧化应激损伤具有浓度依赖性的抑制作用,并抑制α-synuclein的过表达,提示1,5-diCQA对帕金森病细胞模型具有保护作用。

英文摘要：

Objective To investigate the protective effects of 1,5 dicaffeoylquinic acid（1,5-diCQA）preconditioning on the injury of PC12 cells induced by MPP^＋ and the possible mechanisms. Methods MPP^＋ was added to make a model of Parkinson disease in rat pheochromocytoma（PC12） cells. PC12 cells were divided into three groups randomly ： control group, MPP^＋ group, 1,5-diCQA＋MPP^＋ group. Cell viability was determined by MTT assay. Cellular ROS and GSH were observed by a spectrophotometer. The expression of α-synuclein mRNA and protein was detected by using RT-PCR and Western blot respectively. Results ①The cell viability in MPP^＋ group was obviously less than in control group and 1,5-diCQA pretreatment＋ MPP^＋ group. ②The ROS production and cellular depletion was lessened by pretreatment of 1,5-diCQA in a dose-dependent manner. ③1,5-diCQA（50 μmol/L）pretreatment could inhibit the MPP^＋-induced up-regulation of the expression of α-synuclein mRNA and protein. Conclusion 1,5-diCQA may have a neuroprotective potential for it could attenuate the oxidative stress and α-synuclein overexpression in the PC12 cells induced by MPP^＋.