NO前药JS-K对HL-60细胞增殖、分化的影响

Effects of NO prodrug JS-K on HL-60 cell proliferation and differentiation

目的观察一氧化氮前体药物JS-K对白血病HL-60细胞增殖分化的影响。方法体外传代培养HL-60细胞,用不同浓度的JS-K处理HL-60细胞24～96h,MTT法测定细胞活力,观察细胞生长情况。流式细胞仪检测细胞分化的表面分子变化。结果按对数浓度差0.5的间距加入JS-K0.3～10μmol.L-1,处理24～96h,随着JS-K浓度的增加和作用时间的延长,MTT法检测所得各组的光密度值呈剂量依赖性和时间依赖性降低,细胞生长抑制率增高,JS-K作用96h抑制HL-60细胞增殖的IC50为(1.025±0.23)μmol.L-1。JS-K3和10μmol.L-1处理96h后,显微镜下可见细胞数量明显减少,细胞皱缩、细胞碎片明显增加。JS-K3μmol.L-1作用96h后,表达CD11b阳性和CD14阳性细胞的百分率明显提高。结论JS-K可明显抑制HL-60细胞的增殖,促进HL-60细胞分化。

Aim To investigate effects of JS-K on human leukemic cell （HL-60） proliferation and differentiation. Methods JS-K was used to provide nitric oxide in vitro, cell proliferation was measured by MTT method, and the inhibition percentage （IP） of growth was calculated. Cell morphologic changes were observed through light microscopy. Flow cytometer （FCM） was used to evaluate cellular surface molecular of cell differentiation. Results JS-K （ 0. 3 - 10. 0 μmol.L^-1） decreased OD values of HL-60 ceils by MTT method in a time-dependent and dose-dependent manner. The 50% inhibition concentration was 1.23 ±0. 23μmol.L^-1 And the IP of HL-60 cells growth increased. After treatment with JS-K at the concentration 3.0 μmol.L^-1 for 96 hours, the percentages of expressing CD11 b and CD14 positive cells were signifi- cantly increased, the CD11 b expression percentage was 81.70% ± 11.54% , CD14 expression rate was 84. 80% ± 10. 36%. Conclusions JS-K not only inhibits HL-60 cell growth, but also induces cell differentiation.