罗格列酮抑制HL-60细胞增殖和诱导分化作用  

Effects of rosiglitazone on proliferation and differentiation of HL-60 cell

作　　者：戴文香[1] 曹建国[2] 庄英帜[1] 周亭芳[1] 

机构地区：[1]南华大学第一附属医院肿瘤内科,湖南衡阳421001 [2]南华大学肿瘤研究所

出　　处：《临床血液学杂志》2006年第5期272-275,共4页Journal of Clinical Hematology

摘　　要：目的：研究罗格列酮对人急性髓性白血病细胞（HL-60）增殖和诱导分化的作用。方法：用不同浓度的罗格列酮处理HL-60细胞24～72h，MTT观察细胞的增殖抑制作用，瑞特-姬姆萨染色法及硝基蓝四氮（NBT）还原比色法测定细胞分化，流式细胞仪检测细胞周期分布和凋亡率，免疫组化检测PPAR-7表达。结果：不同浓度罗格列酮处理细胞后，HL-60细胞增殖明显受抑，抑制率最高达77％，抑制作用呈现时间、剂量和效应依赖性；细胞周期分析，罗格列酮能诱导HL-60细胞G1期阻滞；同时罗格列酮能促进HL-60细胞分化。免疫组化发现，HL-60细胞表达PPAR-γ，罗格列酮作用HL-60细胞后，发生核转位现象。结论：罗格列酮能抑制HL-60细胞增殖，诱导细胞分化和细胞周期G1期阻滞，其作用机制可能与激活PPAR-γ有关。Objective：To investigate effects of rosiglitazone on human leukemic cell （HL-60） proliferation and differentiation. Method：After treated with rosiglitazone at different dosages, the cell cytotoxic effect was evaluated by MTT. The cell differentiation was examined with Wright-Giemsa and NBT reduction test. The distribution of cell cycle and apoptosis was examined by flow cytometry （FCM）. Expression of PPAR-y was examined by SP im- munocytochemicalstain. Result： Rosiglitazone could inhibit the proliferation of HL-60 cell significantly and 77% percent of cells were inhibited after treated with 100 μmol/L rosiglitazone. Meanwhile, Rosiglitazone could induce differentiation and apoptosis of HL-60 cell. Furthermore, Rosiglitazone could arrest HL-60 cell in G0/G1 phase. PPAR-γ was expressed in HL-60 cells. Treatment with Rosiglitazone caused the nuclear translocation. All these effects of Rosiglitazone were in a dose and time-dependent manner. Conclusion：Rosiglitazone has the capabilities of inhibiting proliferation, inducing differentiation, arresting HL-60 cells at G0/G1 phase of cell cycle. These effects maybe correlate with activation of PPAR-γ.

关 键 词：罗格列酮 HL-60细胞 增殖抑制 分化 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学]