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目的 研究左旋多巴 (L- dopa)对 PC1 2细胞的凋亡诱导作用及诱导机制 ,并探讨其临床意义。方法 以 PC1 2细胞为多巴胺 (DA)神经元的细胞模型 ,用流式细胞术及共焦镜等技术检测不同浓度 L- dopa所致的凋亡率以及胞浆 Ca2 +浓度、p H值的改变。结果 50μmol/ L、1 0 0μmol/ L、1 50μmol/ L处理组凋亡率分别为 1 2 .4%、2 4 .4%、37.2 % ;1 50μmol/ L L- dopa处理后 ,细胞浆 Ca2 + 浓度升高 ,p H值下降。结论 L- dopa可以诱导 PC1 2细胞凋亡 ,呈明显量效关系 ,提示 L- dopa可能会通过凋亡这条途径损害 DA神经元 ,导致疗效减退 ,其机制可能是通过胞浆 Ca2 + 浓度升高或胞浆酸化介导细胞凋亡。
Objective To study the apoptosis-inducing effect and its induction mechanism of L-dopa on PC12 cells and to explore its clinical significance. Methods PC1 2 cells were used as the cell model of dopamine (DA) neurons. Flow cytometry and confocal microscopy were used to detect the apoptotic rate and cytosolic Ca2 + concentrations and p H values induced by different concentrations of L-dopa change. Results The apoptotic rates of 50μmol / L, 100μmol / L and 150μmol / L groups were 12.4%, 24.4% and 37.2%, respectively. After treated with 50μmol / L L-dopa, Concentration increased, p H decreased. Conclusion L-dopa can induce the apoptosis of PC12 cells in a dose-dependent manner, which suggests that L-dopa may damage DA neurons through apoptosis, leading to the diminished therapeutic effect. The mechanism may be that Ca2 + concentration increases High or cytoplasmic acidification mediates apoptosis.