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目的 探讨多巴胺 (DA)诱导大鼠嗜铬细胞瘤细胞株 (PC12 )细胞凋亡的机制。 方法 采用 PC12细胞为模型 ,以 0 .45 mmol/ L的 DA来诱导细胞凋亡的发生 ,用流式细胞仪检测 PC12细胞的亚二倍体峰 ,按 Griess法测定 NO代谢产物 NO2 -的浓度 ,用 Ac- DEVD- AMC为酶作用底物 ,在荧光分光光度计下检测 CPP32活力。 结果 DA处理组的凋亡率为 5 4.49%± 1.6 0 % ,与阴性对照组 (1.6 1%± 0 .18% )比较差异有显著性 (P<0 .0 1) ;NO2 -浓度的升高和 CPP32活化程度与阴性对照组比较差异亦有显著性 (P<0 .0 1)。 结论 CPP32的激活是 DA诱导 PC12细胞凋亡的重要通路 ,而合成增多的 NO可能是 DA激活 CPP32的信号传递分子。
Objective To investigate the mechanism of dopamine (DA) -induced apoptosis in rat pheochromocytoma cell line (PC12). Methods PC12 cells were used as the model to induce the apoptosis of PC12 cells with DA at 0.45 mmol / L. The subdiploid peak of PC12 cells was detected by flow cytometry. The concentration of NO2 - was determined by Griess method , Using Ac-DEVD-AMC substrate for the enzyme, CPP32 activity was measured under a fluorescence spectrophotometer. Results The apoptosis rate of DA group was 5 4.49% ± 1.6 0%, which was significantly different from that of negative control group (1.6 1% ± 0.18%) (P <0.01). The NO 2 - There was also a significant difference between high and CPP32 activation level and negative control group (P <0.01). Conclusion Activation of CPP32 is an important pathway of DA-induced apoptosis in PC12 cells. However, the increased synthesis of NO may be the signal transduction molecule of DA-activated CPP32.