摘要
目的:探讨三七皂苷R1诱导HL-60细胞凋亡的作用机制。方法:采用MTT比色法观察三七皂苷R1对人白血病细胞株HL-60细胞增殖的抑制作用。采用流式细胞术检测细胞凋亡改变,并以RT-PCR检测凋亡调节基因p53、Bcl-2的表达。结果:三七皂苷R1能明显抑制人白血病细胞株HL-60细胞的生长,且呈时间和浓度依赖性。三七皂苷R1作用后人白血病细胞株HL-60细胞呈现凋亡特征,流式细胞术显示凋亡细胞比例升高。RT-PCR检测可见p53mRNA表达显著增加,而Bcl-2mRNA表达减少。结论:三七皂苷R1能诱导人白血病细胞株HL-60细胞凋亡,其作用可能与凋亡调节基因p53的上调和Bcl-2的下调有关。
OBJECTIVE： To study the effects and possible mechanisms of the apoptosis of HL-60 cells induced by notoginsen oside Ri. METHODS： Growth inhibition was measured by methyl thiazolyl tetrazolium （MTT） assay. Apoptosis was detected by flow cytometry. The expression of apoptosis-reguLated gene p53, Bcl-2 was analyzed hy RT PCR. RESULTS： notoginsenoside RI inhibited the growth of human leukemia HL 60 ceils in a dose and time-dependent manner. The cells treated with notoginsenoside R I had the characteristics of apoptosis, increment of apoptotic propor tion with flow cytometry. RT-PCR showed that the expression of p53 gene was apparently increased by notoginsenoside RI, whereas the expression of Bcl 2 gene was reduced. CONCLUSION： notogin senoside R1 can induce apoptosis of human leukemia HL-60 ceils in vitro, which may be mediated by up regul.ating the apoptosis regu Lated gene p53 and down regulating the apoptosis-rcguLated gene survivin, Bcl-2.
出处
《中华肿瘤防治杂志》
CAS
2007年第9期670-672,共3页
Chinese Journal of Cancer Prevention and Treatment
