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背景与目的:三氧化二砷(arsenictrioxide,As2O3)已作为治疗实体瘤的新药应用于临床,但其作用机理仍不清楚。本研究拟探讨As2O3通过线粒体依赖性凋亡通路介导喉癌细胞及其耐药株细胞凋亡的作用。方法:采用MTT法测定As2O3对喉癌细胞KB及其耐药细胞KBv200的细胞毒作用;用AnnexinVFITC染色法检测凋亡早期细胞;细胞线粒体跨膜电位(ΔΨm)用DiOC6标记,流式细胞仪检测。结果:As2O3对KB及KBv200细胞的生长有明显的抑制作用,IC50分别为(0.22±0.02)μg/ml和(0.20±0.01)μg/ml。用AnnexinVFITC染色检测到As2O3呈时间依赖性介导细胞凋亡,2.5μg/mlAs2O3处理24h、48h,KB细胞凋亡率分别为(20.2±3.1)%和(52.2±11.0)%;KBv200细胞凋亡率分别为(15.8±1.3)%和(36.4±5.9)%。2.5μg/mlAs2O3作用于KB与KBv200细胞,ΔΨm降低呈时间依赖性。结论:ΔΨm降低在As2O3诱导喉癌细胞凋亡过程中起着重要的作用。
BACKGROUND & AIM: Arsenictrioxide (As2O3) has been used clinically as a new drug for the treatment of solid tumors, but its mechanism of action remains unclear. This study was to investigate the role of As2O3 in the apoptosis of laryngeal carcinoma cells and its multidrug-resistant cells through mitochondria-dependent apoptosis pathway. Methods: MTT assay was used to determine the cytotoxic effect of As2O3 on KB cells and KBv200 cells. The apoptotic cells were detected by AnnexinVFITC staining. The mitochondrial transmembrane potential (ΔΨm) was detected by flow cytometry . RESULTS: As2O3 significantly inhibited the growth of KB and KBv200 cells with IC50 of (0.22 ± 0.02) μg / ml and (0.20 ± 0.01) μg / ml, respectively. Apoptosis was mediated by AnnexinVFITC in a time-dependent manner. The apoptotic rates of KB cells treated with 2.5μg / ml As2O3 for 24 and 48 hours were (20.2 ± 3.1)% and (52.2 ± 11.0)%, respectively. The apoptosis of KBv200 cells Rates were (15.8 ± 1.3)% and (36.4 ± 5.9)%, respectively. 2.5μg / mlAs2O3 treated KB and KBv200 cells, ΔΨm decreased in a time-dependent manner. Conclusion: The decrease of ΔΨm plays an important role in the apoptosis of laryngeal carcinoma cells induced by As2O3.