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目的:探讨硫化砷在诱导急性非淋巴细胞白血病(APL)细胞株HL-60凋亡的同时,对端粒酶活性的影响及作用机制。方法:采用PCR-ELISA法测定端粒酶活性;半定量RT-PCR检测hTERT mRNA的表达;流式细胞仪分析细胞周期、细胞 凋亡及CD11b表达。结果:用0.3-0.6 mg/L的硫化砷作用72 h,不能诱导HL-60细胞凋亡,将剂量增至1.5-3.0 mg/L时,凋亡细胞的比率逐渐增高,同时伴随HL-60细胞端粒酶活性和hTERT mRNA表达受抑。随着硫化砷浓度的增高,HL-60细胞在G2/M期的比率渐增高。3.0 mg/L的硫化砷作用72 h,HL-60细胞CD11b的表达由1.27％升至6.07％。结论:硫化砷在诱导HL-60细胞凋亡的同时,下调其端粒酶活性。G2/M期细胞比率的增高可能与端粒酶活性降低相关。高浓度硫化砷72 h可轻度诱导HL-60细胞分化。
Aims: To investigate the effect of arsenic sulfide on the apoptosis of acute lymphoblastic leukemia (APL) cell line HL-60 and its effect on telomerase activity and its mechanism. Methods: The telomerase activity was determined by PCR-ELISA. The expression of hTERT mRNA was detected by semi-quantitative RT-PCR. The cell cycle, apoptosis and CD11b expression were analyzed by flow cytometry. Results: Arsenic stress of 0.3-0.6 mg / L for 72 h did not induce apoptosis of HL-60 cells. When the dose was increased to 1.5-3.0 mg / L, the apoptotic cells increased gradually, accompanied by HL-60 Cell telomerase activity and hTERT mRNA expression was suppressed. As the concentration of arsenic sulfide increased, the ratio of HL-60 cells in G2 / M phase gradually increased. In the presence of 3.0 mg / L arsenic sulfide for 72 h, the expression of CD11b in HL-60 cells increased from 1.27% to 6.07%. Conclusion: Arsenic sulfide can down-regulate telomerase activity while inducing HL-60 cell apoptosis. Elevated G2 / M cell ratio may be associated with decreased telomerase activity. High concentrations of arsenic sulfide 72 h mildly induce HL-60 cell differentiation.