【摘要】 目的:观察胆固醇合成抑制剂洛伐他汀(lovastatin,LOV)对HL60、KG1、K562白血病细胞增殖、凋亡的影响,并进一步探讨其作用机制。方法:首先利用MTT法、台盼蓝拒染法观察LOV对HL60、KG1、K562细胞增殖及活力的影响。再通过细胞形态观察,DNA凝胶电泳,流式细胞术分析,RTPCR半定量测定bcl2mRNA水平等技术,系统观察LOV对HL60、KG1、K562体外诱导凋亡的情况。结果:①LOV抑制HL60、KG1、K562细胞增殖,IC50分别为17.16、51.65、58.95μmol/L;②LOV诱导HL60、KG1、K562细胞凋亡,影响细胞周期进程,细胞阻滞于G1/S期;LOV在诱导HL60细胞凋亡过程中随作用时间延长,bcl2表达水平逐渐下降。结论:LOV抑制HL60、KG1、K562细胞增殖并诱导凋亡,阻滞细胞周期进程于G1/S期;bcl2参与了LOV诱导凋亡的基因调控。更多还原

【Abstract】 Objective: To investigate the effect of lovastatin (LOV), a cholesterol synthesis inhibitor on the cell growth and apoptosis in HL 60, KG 1, K562 cells and elucidate its mechanism. Methods: Cell proliferation and viability were analyzed firstly by MTT assay and trypan blue exclusion assay. Cell morphological analysis,DNA electrophoresis,flow cytometry and semi quantitative RT PCR were performed to determine whether LOV could induce apoptosis of HL 60, KG 1, K562 cells in vitro. Results: ①LOV inhibited HL 60, KG 1, K562 cells growth with the IC50 of 17.16, 51.65, 58.95 μmol/L, respectively. ②LOV induced apoptosis in HL 60, KG 1, K562 cells and affected the cell cycle progression; most of cells were arrested in G1/S phase; bcl 2 mRNA was down regulated by LOV in a time depended manner. Conclusion: LOV can inhibit proliferation, induce apoptosis,and interfere with cell cycle progression in HL 60, KG 1, K562 cells. bcl 2 may be involved in the gene regulation of the LOV induced apoptosis.更多还原