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目的：探讨三氧化二砷（Ａｓ_２Ｏ_３）治疗白血病的疗效机理。方法：以 ＨＬ－６０细胞株为体外模型，终浓度为０．２０μｍｏｌ／Ｌ Ａｓ２_Ｏ_３作用２４、４８ｈ后，用ＰＩ／ＡｎｎｅｘｉｎＶ－ＦＩＴＣ双标记，流式细胞术观察Ａｓ_２Ｏ_３对ＨＬ－６０细胞凋亡及其对细胞株端粒酶活性的影响。结果：Ａｓ２_Ｏ_３作用于ＨＬ－６０细胞后ＰＩ阴性／ＡｎｎｅｘｉｎＶ－ＦＩＴＣ阳性细胞增多，提示细胞发生凋亡，ＤＮＡ周期分析显示主要作用在细胞Ｇ_２－Ｍ期，４８ｈ对端粒酶有轻微抑制作用。结论：Ａｓ_２Ｏ_３主要通过诱导细胞凋亡杀伤白血病细胞。
Objective: To investigate the therapeutic mechanism of arsenic trioxide (As_2O_3) in the treatment of leukemia. METHODS: HL-60 cell line was used as an in vitro model. The final concentration of As2O3 was 0.20 μmol/L for 24 and 48 h. PI/Annexin V-FITC double labeling and flow cytometry were used to observe the apoptosis of HL-60 cells induced by As 2 O 3. Its effect on the telomerase activity of cell lines. RESULTS: As2_O_3 acted on PI-negative/AnnexinV-FITC-positive cells in HL-60 cells, suggesting that apoptosis occurred in the cells. DNA cycle analysis showed that the cells mainly acted in the G2-M phase, and slightly inhibited telomerase activity at 48 h. CONCLUSION: As2O3 mainly kills leukemia cells by inducing apoptosis.