三氧化二砷诱导K562/ADM细胞凋亡的作用机制研究

目的 观察三氧化二砷(As2O3) 对K562/ADM细胞的诱导凋亡效应, 探讨其作用机制。 方法 应用噻唑蓝(MTT) 比色法、Wright-Giemsa 染色、DNA 琼脂糖凝胶电泳和流式细胞术(FCM) 观察K562/ADM 细胞凋亡;FCM 测定K562/ADM 细胞Fas、Bcl-2、P53 蛋白水平的变化;比色法检测Caspase3 活性变化。 结果 As2O3 可抑制K562/ADM 细胞增殖;K562/ADM 呈典型凋亡形态改变;DNA 电泳可见梯状条带出现;FCM 分析示亚G1 期细胞比例增高, G2 M 期阻滞;Fas、P53 蛋白表达明显上调;Caspase3 活性明显增强。 结论 A_s2O₃ 可通过Fas 依赖性Caspase3 激活而诱导K562/ADM 细胞凋亡。

Arsenic trioxide-induced apoptosis in K562/ADM cells and its mechanisms

AIM: To observe the apoptosis of K562/ ADM cells induced by As2O3 and to explore its possible mechanisms. METHODS: MTT assay, Wright-Giemsa staining, DNA agarose gel electrophoresis and cell cycle analysis were used to examine apoptosis in K562/ADM cells.Expression levels of Fas, Bcl-2 and P53 antigens were measured with FCM.Colorimetric assay was employed to detect the activation of Caspase3. RESULTS: As2O3 inhibited growth of K562/ADM cells.Morphological changes typical of apoptosis were observed through light microscopy.Agarose gel electrophoresis showed evident DNA fragmentation.Cell cycle analysis indicated increased Sub-G1 proportion and apoptosis rate, as well as apparent G2 M phase arrest.The expression of Fas and P53 antigens significantly increased after application of As2O3.Caspase 3 was also activated by As2O3. CONCLUSION: As2O3 induces apoptosis in K562/ADM cells by activating Caspase 3 via a Fas-dependent pathway.