中文摘要：

目的：研究电压门控性钾通道在急性髓系白血病（ acute myelocytic leukemia ，AML）细胞增殖及凋亡中的作用。方法通过台盼蓝拒染法检测AML细胞株THP-1生存活力；应用Annexin V／PI双标法和DAPI荧光染色法检测细胞凋亡；应用流式细胞术检测[ Ca2＋] i变化。结果电压门控性钾通道抑制剂4-氨基吡啶（4-aminopyrine，4-AP）作用72 h后，THP-1细胞生存活力明显下降，IC50为3.68 mmol／L。药物作用72 h 后， DAPI 荧光染色示4-AP 2 mmol／L 组、4 mmol／L 组细胞凋亡率分别为（14.38±1.82）％、（32.91±3.47）％，与对照组（6.35±0.29）％比较差异显著（P＜0.05）；Annexin V／PI双标记法示4-AP 2 mmol／L组、4 mmol／L组细胞凋亡率分别为（16.89±2.49）％、（38.26±4.03）％，与对照组（6.06±0.32）％比较差异均显著（P＜0.05）。2及4 mmol／L 4-AP作用1 min后，THP-1细胞内Fluo-3／AM荧光强度分别为（378.36±10.84）、（391.31±24.78），与对照组（57.24±7.18）相比具有显著性差异（ P＜0.05）。结论电压门控性钾通道阻滞剂4-AP抑制AML细胞生存活力并可诱导其凋亡，提示电压门控性钾通道可能是AML治疗的潜在靶点。

英文摘要：

Objective To investigate the effect of voltage-gated potassium channel on the cell cycle and apoptosis of acute myeloid leukemia （ AML）.Methods The effects of AML cell lines THP-1 on cells survival were determined by Trypan blue exclusion .The apoptosis rate was analyzed by using Annexin V-FITC double labeling and DAPI assay .The level of intracellular free Ca2＋was observed by flow cytometry .Resul ts THP1-cell viability was significantly de-creased with 4-aminopyridine treatment for 72 h, IC50 was 3.68 mmol/L.After 72 h, DAPI staining showed that the apoptosis rate of THP-1 in 4-AP 2 mmol/L group and 4 mmol/L group were （14.38 ±1.82）%and （32.91 ±3.47）%respectively, and were all significantly larger＆nbsp;than that of the control group （6.35 ±0.29 ） , P〈0.05 .Annexin V-FITC/PI double staining showed that the apoptosis rate of THP-1 were （16.89 ±2.49）%and （38.26 ±4.03）%respec-tively, and were all significantly larger than that of the control group （6.06 ±0.32）, P〈0.05. After 1 min, the Fluo-3/AM fluorescence intensity of THP-1 cell lines in 4-AP 2 mmol/L group and 4 mmol/L group were （378.36 ±10.84 ） and （391.31 ±24.78 ） respectively,and were all significantly larger than that of the control group （57.24 ±7.18 ） , P〈0.05 .Conclusion 4-AP could decrease the ability of cell growth and apoptosis of AML cells by blocking the voltage-gated potassium channel , which provides new ideas in the targeted therapy of AML .