摘要
目的探讨左旋多巴(L-dopa)治疗帕金森病(PD)疗效减退的机制。方法以PC12(大鼠肾上腺嗜铬细胞瘤)细胞为多巴胺(DA)神经元的细胞模型,应用流式细胞术(FCM)、DNA琼脂糖凝胶电泳、透射电镜、碘化丙啶(propidiumiodide,PI)/HO33342双染色法观察L-dopa对PC12细胞凋亡的影响,每组样本数为7。结果对20μmol/LL-dopa处理组的凋亡率2.5%与对照组2.3%比较无显著差异(P>0.05),但50、100、150μmol/L的L-dopa作用24小时所致的凋亡率分别为12.4%、24.4%、37.2%,与对照组比较差异有非常显著意义(P<0.01)。结论在一定浓度范围内的L-dopa可以诱导PC12细胞凋亡,提示凋亡可能参与了L-dopa治疗PD疗效减退的病理过程。
Objective To explore the mechanism of the decline in effectiveness during the treatment ofParkinson's disease with L-dopa. Methods In this study, we used flow cytometry、agarose gel electrophoresis,electron microscopy and PI/HO33324 double staining to detect the induction of apoptosis of the catecholaminergicPC12 cells ny L-dopa. Results The ratios of apoptosis induced by L-dopa at the mranges of the contents of 50,100and 150 μmol/L were 12. 4%, 24.4%, 37. 2% respectively; significantly higher than those of the control group(P<0.01), while the ratio of apoptosis induced by L-dopa at the concentration of 20μmol/L was similar withthat of the controls (P>0. 05).Conclusion The results suggested that apoptosis might be involved in thepathogenetic phase, when the effectiveness of the treatment with L-dopa was declining.
出处
《中华神经科杂志》
CAS
CSCD
1999年第5期284-286,共3页
Chinese Journal of Neurology