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目的:探讨咖啡酸苯乙酯(Caffeic Acid Phenethyl Ester,CAPE)对神经毒素诱导的帕金森病模型神经元损伤的保护作用。方法:体外用MPP+处理PC12细胞制作PD细胞模型,利用MTT法和流式细胞仪分别测定细胞存活率和细胞凋亡。将C57BL雄性小鼠用MPTP处理(20 mg/kg,3次,ip)制作PD小鼠模型,用尼氏染色检测黑质致密区神经细胞数,免疫组化方法检测黑质致密区酪氨酸羟化酶(TH)和Caspase-3阳性细胞数。结果:PC12细胞中,1.25μM的CAPE可以显著抑制MPP+诱导的细胞活性的丧失和细胞凋亡。PD小鼠模型中,MPTP模型组黑质致密区神经细胞数和TH阳性细胞数较正常对照组明显降低,黑质致密区Caspase-3阳性细胞数较正常对照组明显增加。CAPE(50 mg/kg,ip,7d)可以显著增加黑质致密区TH阳性细胞数,减少黑质致密区Caspase-3阳性细胞数。结论:CAPE对神经毒素诱导的PD模型神经元损伤有明显的保护作用。
Objective: To investigate the protective effect of Caffeic Acid Phenethyl Ester (CAPE) on neuronal damage induced by neurotoxin in Parkinson’s disease model. Methods: PC12 cells were treated with MPP + in vitro to produce PD cell model. Cell viability and apoptosis were determined by MTT assay and flow cytometry respectively. The C57BL male mice were treated with MPTP (20 mg / kg, 3 times, ip) to make the PD mouse model. The number of neurons in substantia nigra was detected by Nissl staining. The tyrosine Hydroxylase (TH) and Caspase-3 positive cells. Results: In PC12 cells, 1.25μM CAPE significantly inhibited MPP + -induced loss of cell viability and apoptosis. In the PD mouse model, the numbers of neuronal cells and TH positive cells in substantia nigra compact zone in MPTP model group were significantly lower than those in normal control group, and the number of Caspase-3 positive cells in substantia nigra compact zone was significantly higher than that in normal control group. CAPE (50 mg / kg, ip, 7d) could significantly increase the number of TH positive cells in substantia nigra compact zone and decrease the number of Caspase-3 positive cells in substantia nigra compact zone. CONCLUSION: CAPE can protect neurons from neurotoxicity induced PD model.