曲古抑菌素A诱导HL-60细胞凋亡机制的研究  

Apoptosis mechanism of HL-60 cells induced by TSA

作　　者：杨炜华[1] 温培娥[1] 范华[1] 赵海涛[1] 乔高娟[1] 任霞[1] 任海全[1] 唐天华[1] 姜国胜[1] 

机构地区：[1]山东省医学科学院基础医学研究所山东省现代医用药物与技术重点实验室山东省医药卫生肿瘤免疫与中药免疫重点实验室,山东济南250062

出　　处：《中华肿瘤防治杂志》2009年第4期249-251,255,共4页Chinese Journal of Cancer Prevention and Treatment

基　　金：国家自然科学基金(30771103);科技部中瑞政府间合作项目(AM15B:18);山东省自然科学基金重点项目(Z2004C08);山东省1020工程杰出学科带头人基金;济南市国际合作重点项目(063306)

摘　　要：目的:探讨曲古抑菌素A(TSA)在体外诱导急性早幼粒白血病HL-60细胞凋亡的机制。方法:采用MTT方法检测TSA对HL-60细胞增殖的影响,流式细胞术检测细胞周期和细胞凋亡,RT-PCR检测凋亡相关基因Bax、Caspase-9和Caspase-3的表达。结果:0.1μmol/L的TSA可明显抑制细胞增殖,P<0.01;0.05μmol/L的TSA可使细胞周期阻滞在G0/G1期(P<0.05),但0.1μmol/L的TSA才能引起细胞凋亡(P<0.01);经0.1μmol/L的TSA作用12 h后,Bax、Caspase-9和Caspase-3基因表达明显升高,P<0.01。结论:TSA诱导HL-60细胞凋亡的机制在于引起细胞周期阻滞,上调Bax、Caspase-9和Caspase-3的表达。OBJECTIVE： To explore the apoptosis mechanism of HL-60 cell induced by TSA. METHODS： The MTT method was used to test HL-60 cell growth. The cell cycle and apoptosis were tested by FCM. Semi-quantitative RT-PCR was used to detect the mRNA expressions of Bax, Caspase-9 and Caspase-3 in the cells treated by TSA. RESULTS： A decrease in cell growth was observed when the cells were treated by 0.1 μmol/L TSA, P〈0.01. The cells were significantly accumulated at the G0/G1 phase under the treatment of 0.05 9mol/L TSA （P〈0.05）. However, the But cell apoptosis was only observed when the concentration of TSA was over 0. 1 μmol/L（P〈0.01）. The expressions of Bax, Caspase 9 and Caspase-3 were up regulated by the exposure of HL-60 cells to 0.1 μmol/L TSA for 12 hours,P〈0. 01. CONCLUSION： The mechanism of HL-60 cell apoptosis induced by TSA is related to the up-regulation of Bax, Caspase-9 and Caspase-3.

关 键 词：白血病 早幼粒细胞 急性/病理学 抗肿瘤药/药理学 半胱氨酸天冬氨酸蛋白酶 细胞凋亡 

分 类 号：R733.7[医药卫生—肿瘤]