Desipramine antagonized corticosterone-induced apoptosis in cultured PC12 cells  

地昔帕明对皮质酮诱导培养的PC12细胞调亡的拮抗作用(英文)

作　　者：李云峰 罗质璞[1] 

机构地区：[1]军事医学科学院毒物药物研究所,北京中国100850

出　　处：《Acta Pharmacologica Sinica》2002年第4期311-314,共4页中国药理学报（英文版）

摘　　要：AIM: To study possible action mechanism of a tricyclic antidepressant, desipramine (DIM). METHODS: Cultured PC12 cells were exposed to corticosterone in the absence or presence of DIM for 5 d. Agarose gel electrophoresis, flow cytometry, and electron microscopy were used to detect the apoptosis of PC12 cells. RESULTS: Corticosterone 10 μmol/L treatment for 5 d elicited typical apoptotic biochemical and morphological changes including condensed chromatin shaped like crescent moon, nuclear fragmentation, and DNA degradation. The highest percentage of apoptotic cells accumulated to 28 % ±9 % . Agarose gel electrophoresis showed typical DNA ladders pattern. While in the presence of DIM 1 or 5μmol/L, apoptosis percentage was markedly decreased with lightened DNA ladder and ultrastructure of the cells was improved. CONCLUSION: DIM could antagonize the apoptosis in PC12 cells induced by corticosterone, which may be one of the cellular mechanisms of its antidepressant effect.目的:探讨三环类抗抑郁剂的作用机制.方法:运用DNA电泳法、流式细胞仪法、电镜法检测了皮质酮诱导的PC12细胞凋亡并观察了去甲丙米嗪(DIM)的效应 结果:皮质酮10μmol/L处理5d可显著诱导PC12细胞凋亡,凋亡发生率最高达(28±9)％,DNA电泳图谱则表现出典型的梯状条带,DIM的1和5μmol/L使凋亡发生率明显降低并使梯状条带变浅、减轻,细胞的超微结构也有明显改善.结论:DIM对皮质酮诱导的PC12细胞凋亡有拮抗作用,这可能是其抗抑郁效应的细胞机制之一.

关 键 词：DESIPRAMINE antidepressive agents CORTICOSTERONE PC12 cells APOPTOSIS 

分 类 号：R96[医药卫生—药理学]