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目的:对比硫化砷对慢性粒细胞白血病细胞株K562和急性早幼粒细胞白血病细胞株NB4两种细胞的作用是否存在差异及其机制。方法:PCR-ELISA法测定端粒酶活性;半定量RT-PCR检测hTERTmRNA的表达;流式细胞术测量细胞周期、凋亡。结果:0.15～0.6mg/L硫化砷(72h)可在诱导NB4细胞凋亡的同时,下调细胞端粒酶活性和hTERT-mRNA表达,同样作用对于K562细胞需要硫化砷浓度达到0.3～3mg/L。0.3mg/L硫化砷(72h)可引起NB4细胞出现G2/M期细胞比例增高。而K562细胞需要在1.5mg/L硫化砷诱导下出现G2/M期细胞比例增高。结论:端粒酶系统可能是硫化砷诱导NB4和K562细胞凋亡的途径之一;由硫化砷诱导的G2/M期阻滞可能与端粒酶活性的显著下降相关。NB4和K562细胞对硫化砷的敏感性存在明显差异,具体机制有待进一步研究。
Aims: To compare the effects of arsenic sulfide on the two cell lines of chronic myeloid leukemia K562 and acute promyelocytic leukemia NB4 cells and its mechanism. Methods: The telomerase activity was determined by PCR-ELISA. The expression of hTERT mRNA was detected by semi-quantitative RT-PCR. Cell cycle and apoptosis were measured by flow cytometry. Results: Arsenic sulfide (0.15-0.6 mg / L) induced apoptosis of NB4 cells at the same time, down-regulated the telomerase activity and hTERT-mRNA expression. The same effect required arsenic sulfide concentration of 0.3-3 mg / L for K562 cells . 0.3mg / L arsenic sulfide (72h) can cause NB4 cells appear G2 / M phase cells increased. However, K562 cells need G2 / M phase cells induced by 1.5mg / L arsenic sulfide. CONCLUSION: The telomerase system may be one of the pathways that lead to apoptosis in NB4 and K562 cells. Arsenic sulfide-induced G2 / M arrest may be related to the significant decrease of telomerase activity. The sensitivity of NB4 and K562 cells to arsenic sulfide has obvious differences, the specific mechanism needs further study.