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【目的】探讨细胞分化剂 (CDA Ⅱ )在三氧化二砷 (As2 O3 )诱导肝癌细胞凋亡效应中的作用。【方法】应用CDA Ⅱ和As2 O3 共同处理肝癌细胞株BEL 74 0 2、HepG2 ,通过四唑蓝比色法检测细胞存活率 ;用活细胞荧光染色观测细胞凋亡及形态学变化、流式细胞术分析细胞周期变化及凋亡率。【结果】CDA Ⅱ毒性作用很低 ,但可以显著增强As2 O3 对肝癌细胞生长的抑制作用 ,1 0 g/LCDA Ⅱ便可使As2 O3 对两株细胞的半数抑制浓度由 5 0 μmol/L降低至 1 0 μmol/L(P <0 0 1)。形态学可观察到CDA Ⅱ明显加强了As2 O3 诱导的细胞凋亡 ,且与剂量有关 ;流式细胞术分析 ,低质量浓度的CDA Ⅱ (<2 0 g/L)细胞生长阻滞于G2 期较对照组多 ,而随着剂量的增加则凋亡细胞和滞留于G1期的细胞增多 ,低剂量CDA Ⅱ与As2 O3 共同处理肝癌细胞后 ,凋亡率明显高于单独用As2 O3 。【结论】CDA Ⅱ可增强As2 O3 诱导肝癌细胞的凋亡效应 ,两药具有协同作用。
【Aim】 To investigate the role of CDA Ⅱ in the apoptosis of hepatoma cells induced by As 2 O 3. 【Method】 The hepatocellular carcinoma cell lines BEL 74 0 2 and HepG2 were co-treated with CDA Ⅱ and As 2 O 3, and the cell viability was detected by tetrazolium blue staining. The apoptosis and morphological changes were observed by fluorescent staining of live cells. Analysis of cell cycle changes and apoptosis rate. 【Results】 The cytotoxicity of CDA Ⅱ was low, but the inhibitory effect of As 2 O 3 on the growth of hepatoma cells was significantly enhanced. When 50 μg / L of LCDA Ⅱ was added, the half inhibitory concentration of As 2 O 3 on both cells decreased from 50 μmol / L To 10 μmol / L (P <0.01). Morphology CDA Ⅱ was observed to significantly enhance As 2 O 3 -induced apoptosis and was dose-dependent. Flow cytometry analysis showed that low-concentration CDA Ⅱ (<20 g / L) cells arrested in G2 phase Compared with the control group, the apoptotic cells and the cells in G1 phase increased with the increase of dose, and the apoptosis rate of hepatoma cells treated with low dose of CDA Ⅱ and As 2 O 3 was significantly higher than that of As 2 O 3 alone. 【Conclusion】 CDA Ⅱ can enhance the apoptosis of HepG2 cells induced by As2 O3. The two drugs have synergistic effects.