【摘要】 目的研究地昔帕明（ＤＭＩ）对大鼠脑胶质瘤Ｃ６的增殖抑制和凋亡诱导作用，为三环类抗抑郁药作为肿瘤辅助治疗提供新的理论和实验依据。方法用ＭＴＴ比色法测定Ｃ６细胞活力，用透射电镜、流式细胞术（ＦＣＭ）检测细胞凋亡，用免疫组化法分析ｂｃｌ－２蛋白的表达。结果ＤＭＩ对Ｃ６细胞的增殖具有明显的浓度依赖性抑制作用， ＩＣ５０（ ９５ ％置信区间）为２０．７（１７．３～２４．２）μｍｏｌ·Ｌ－１，细胞阻滞于Ｇ０～Ｇ１期。ＤＭＩ（４０μｍｏｌ·Ｌ－１）使细胞发生典型的凋亡形态改变，ＤＮＡ含量分析显示 Ｇ０峰左侧出现亚二倍体细胞凋亡峰，呈浓度依赖性，蛋白合成抑制剂ＣＨＸ可显著抑制ＤＭＩ诱导的细胞凋亡。同时，ＤＭＩ（１０ μｍｏｌ·Ｌ－１）可下调细胞 ｂｃｌ－２蛋白的表达。结论ＤＭＩ体外对Ｃ６细胞的增殖具浓度依赖性抑制作用，并诱导细胞凋亡。更多还原

【Abstract】 AIM To study the effect of desipramine (DMI ) on proliferation inhibition and apoptosis induction of rat glioma C6 cells. METH ODS Cell proliferation was measured by MTT col- orimetric assay and cells undergoing apoptosis were determined by electron microscope and flow cytometry. The expression of hcf-2 was evaluated by immunohistochemistry. RESULTS DMI could result in the concentration- dependent inhibition of C6 cell proliferation and lead to arrest in GO - G1 phase of cell cycle. The value of Ica and 95% confidence limits were 20.7(17 .3~24 .2) μmol·L~ 1. DMI(40 μmol· L-l )-induced apoptosis showed classical apoptotic morphology and the hypodiploid peak appeared on the histogram of FCM in a concentration- dependent man ner, which could be abrogated by cycloheximide(1. 8 μmol· L- １ ). Meanwhile, DMI (10 μmol· L- 1 ) could down-regulate the expression of apoptosis associated gene hcl-2. CONCLUSION DMI could inhibit cell proliferation in a concentration dependent manner and induce typical apoptosis of C6 cells.更多还原