目的：观察三七皂苷（notoginsenoside)R1对白血病细胞株HL-60凋亡的影响，探讨其可能的作用机制。方法：采用MTT法和流式细胞术（Annexin V-FITC双染法）分别检测三七皂苷R1（10、20、40及80 μmol/L）处理HL-60细胞12、24、36及48 h后HL-60细胞的凋亡情况，Western blotting检测HL-60细胞内Bcl-2、Bax及细胞色素C（cytochrome-C，Cyt C)蛋白的表达水平，JC-1染色法观察HL-60线粒体膜电位的变化。结果：MTT和流式细胞术检测显示三七皂苷R1浓度依赖性诱导HL-60细胞的凋亡，且细胞存活率随处理时间的增加而降低；与空白对照组相比，加入三七皂苷R1后细胞中Bcl-2蛋白表达显著减少\[(0.45±0.03) vs (1.00±0.00)，P<0.05\]、Bax蛋白表达显著增加\[(1.72±0.08) vs (1.00±0.00)，P<0.05\]；Bcl-2/Bax比值减小\[(0.21±0.01) vs (1.00±0.00)，P<005\]；线粒体膜电位降低\[(0.56±0.09) vs (1.00±0.00)，P<005\]；胞质（cyto）中Cyt-C蛋白表达水平显著下降\[(0.42±0.03) vs (1.00±0.00)，P<0.05\]。 结论： 三七皂苷R1可显著诱导HL-60细胞凋亡，其作用机制可能是通过线粒体通路促进细胞的凋亡；本实验可为三七皂苷R1用于临床治疗白血病提供实验依据。

Objective:To explore the effect of Notoginsenoside R1 on the apoptosis of human leukemia cell line HL-60 and possible mechanisms. Methods：After HL-60 cells were incubated with different concentrations of Notoginsenoside R1 (10, 20, 40 and 80 μmol/L) for 12, 24, 36 h and 48 h, apoptosis of the HL-60 cells was determined by MTT and Annexin V-FITC flow cytometry assays respectively. The expression of Bcl-2, Bax and cytochrome C (Cyt-C) in the HL-60 cells was determined by Western blotting. The change of mitochondrial membrane potential was assessed by JC-1 dyeing method. Results：The results of MTT and flow cytometry assays showed that Notoginsenoside R1 induced the apoptosis of HL-60 cells in dose-dependent manners, and survival rate of the HL-60 cells decreased with increase of incubation time; after adding Notoginsenoside R1, expression of Bcl-2 protein in the HL-60 cells remarkably decreased (\[0.45±0.03\] vs \[1.00±0.00\]，P<0.05, compared with control group); expression of Bax protein significantly increased (\[1.72±0.08\] vs \[1.00±0.00\]，P<0.05, compared with control group); and the ratio of Bcl-2/Bax decreased (\[0.21±0.01\] vs \[1.00±0.00\]，P<0.05); the mitochondrial membrane potential decreased (\[0.56±009\] vs \[1.00±0.00\]，P<0.05)；and expression level of Cyt-C protein in cytoplasm remarkably decreased (\[0.42±0.03\] vs \[1.00±0.00\]，P<0.05\]. Conclusion：Notoginsenoside R1 can remarkbly incluce apoptosis of HL-60 cells. Mitochondria-dependent pathway may be involved inNotoginsenoside R1-induced apoptosis of HL-60 cells. These findings suggest that Notoginsenoside R1 may be a new strategy for treatment of leukemia.

河北省卫生和计划生育委员会基金资助项目（No.20150238）