中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2001年
2期
161-164
,共4页
祁红%陈红专%冯菊妹%孙玉燕%金正均
祁紅%陳紅專%馮菊妹%孫玉燕%金正均
기홍%진홍전%풍국매%손옥연%금정균
抗抑郁药%地昔帕明%脑胶质瘤%细胞凋亡
抗抑鬱藥%地昔帕明%腦膠質瘤%細胞凋亡
항억욱약%지석파명%뇌효질류%세포조망
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(40 μmol*L-1)使细胞发生典型的凋亡形态改变,D NA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。
目的研究地昔帕明(DMI)對大鼠腦膠質瘤C6的增殖抑製和凋亡誘導作用,為三環類抗抑鬱藥作為腫瘤輔助治療提供新的理論和實驗依據。方法用MTT比色法測定C6細胞活力,用透射電鏡、流式細胞術(FCM)檢測細胞凋亡,用免疫組化法分析bcl-2蛋白的錶達。結果 DMI對C6細胞的增殖具有明顯的濃度依賴性抑製作用,IC50(95%置信區間)為20.7(17.3~24.2)μmol*L-1,細胞阻滯于G0~G1期。DMI(40 μmol*L-1)使細胞髮生典型的凋亡形態改變,D NA含量分析顯示G0峰左側齣現亞二倍體細胞凋亡峰,呈濃度依賴性,蛋白閤成抑製劑CHX 可顯著抑製DMI誘導的細胞凋亡。同時,DMI(10 μmol*L-1)可下調細胞bcl-2蛋白的錶達。結論 DMI體外對C6細胞的增殖具濃度依賴性抑製作用,併誘導細胞凋亡。
목적연구지석파명(DMI)대대서뇌효질류C6적증식억제화조망유도작용,위삼배류항억욱약작위종류보조치료제공신적이론화실험의거。방법용MTT비색법측정C6세포활력,용투사전경、류식세포술(FCM)검측세포조망,용면역조화법분석bcl-2단백적표체。결과 DMI대C6세포적증식구유명현적농도의뢰성억제작용,IC50(95%치신구간)위20.7(17.3~24.2)μmol*L-1,세포조체우G0~G1기。DMI(40 μmol*L-1)사세포발생전형적조망형태개변,D NA함량분석현시G0봉좌측출현아이배체세포조망봉,정농도의뢰성,단백합성억제제CHX 가현저억제DMI유도적세포조망。동시,DMI(10 μmol*L-1)가하조세포bcl-2단백적표체。결론 DMI체외대C6세포적증식구농도의뢰성억제작용,병유도세포조망。
AIM To study the effect of desipramin e (DMI) on proliferation inhibition and apoptosis induction of rat glioma C6 cel ls. METHODS Cell proliferation w as measured by MTT colorimetric assay and cells undergoing apoptosis were determ ined by electron microscope and flow cytometry. The expression of bcl-2 was eva luated by immunohistochemistry. RESULTS DMI could result in the c oncentration-dependent inhibition of C6 cell proliferation and lead to arrest i n G0~G1 phase of cell cycle. The value of IC50 and 95% confidence lim its were 20.7(17.3~24.2) μmol*L-1.DMI(40 μmol*L-1)-indu ced apoptosis showed classical apoptotic morphology and the hypodiploid peak ap peared on the histogram of FCM in a concentration-dependent manner, 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 b cl-2. CONCLUSION DMI could inhibit cell proliferation in a con centration dependent manner and induce typical apoptosis of C6 cells.