p53和Bcl-2 mRNA表达在三七皂苷R1诱导HL-60细胞凋亡中的作用

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p53 mRNA表达显著增加,而Bcl-2 mRNA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.

Expressions of apoptosis-relatedgene p53, Bcl-2 in the notoginsenoside R1 induced apoptosis of HL-60 cells

OBJECTIVE:To study the effects and possible mechanisms of the apoptosis of HL-60 cells induced by notoginsenoside R1.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 by RT-PCR.RESULTS:notoginsenoside R1 inhibited the growth of human leukemia HL-60 cells in a dose-and time-dependent manner.The cells treated with notoginsenoside R1 had the characteristics of apoptosis,increment of apoptotic proportion with flow cytometry.RT-PCR showed that the expression of p53 gene was apparently increased by notoginsenoside R1,whereas the expression of Bcl-2 gene was reduced.CONCLUSION:notoginsenoside R1 can induce apoptosis of human leukemia HL-60 cells in vitro,which may be mediated by up-reguLating the apoptosis-reguLated gene p53 and down-reguLating the apoptosis-reguLated gene survivin,Bcl-2.