摘要
【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。
To illustrate the possible role of cell differential agent Ⅱ (CDA Ⅱ) on the apoptosis of hepatoma cells induced by arsenic trioxide (As 2O 3) Hepatoma cell lines BEL 7402 and HepG2 were treated with As 2O 3 together with CDA Ⅱ Cell surviving fraction was determined by MTT assay; morphological changes were observed by immunofluorescence staining of Hoechst 33 258; cell cycle and the apoptosis index were determined by flow cytometry(FCM) Cytotoxity of CDA Ⅱ is low Nevertheless, CDA Ⅱ could strongly potentiate arsenic trioxide induced apoptosis At 1 0 g/L of CDA Ⅱ, IC 50 of As 2O 3 on hepatoma cell lines was reduced from 5 0 μmol/L to 1 0 μmol/L (P<0 01) The potentiation of apoptosis was dependent on the dosage of CDA Ⅱ FCM study indicated that in hepatoma cell growth was inhibited by CDA Ⅱ at lower concentration (<2 0 g/L) primarily by arresting at S and G 2 phase, and at higher concentrations (>2 0 g/L) apoptotic cell and cell cycle arresting at G 1 phase increased proportionally The combination of two drugs led to much higher apoptotic rates, compared to separate usage of either drug alone [Conclusion] CDA Ⅱ can strongly potentiate As 2O 3 induced apoptosis in hepatoma cells, and two drugs can produce a significant synergic effect
出处
《中山医科大学学报》
CAS
CSCD
北大核心
2002年第6期423-426,T002,共4页
Academic Journal of Sun Yat-sen University of Medical Sciences
基金
广东省科委广东省重点科技攻关科研基金资助项目 (1998110 )
关键词
细胞分化剂
三氧化二砷
肝癌
细胞凋亡
carcinoma,hepatocellular
apoptosis
cell division phase
growth inhibitors
arsenic trioxide
