甲异靛联合imatinib对CML K562细胞的促凋亡作用

Meisoindigo in Combination with Imatinib Accelerates Apoptosis of K562 Cells

目的研究甲异靛联合imatinib促进K562细胞凋亡的作用。方法K562细胞经imatinib或/和甲异靛处理48h后,采用流式细胞术检测细胞凋亡相关指标(线粒体跨膜电位和AnnexinV/PI)的改变,ELISA方法检测caspase3活性改变,Westernblot检测凋亡相关蛋白(cytC,cIAP1,procaspase3和PARP)的改变。结果与单用组相比,20μmol/L甲异靛与0.3μmol/Limatinib联合应用后,线粒体跨膜电位下降细胞比例明显升高,cytC释放入胞浆,caspase3酶原形式procaspase3减少,caspase3活性升高,其底物PARP被降解,AnnexinV水平升高。结论甲异靛与imatinib合用可协同促进K562细胞凋亡。

Objective To investigate whether imatinib in combination with meisoindigo can accelerate apoptosis of K562 cells. Methods After drug treatment alone or combined for 48 h, apoptosis was analyzed by flow cytometry (mitochondrial transmembrane potentials and Annexin V/PI staining), caspase 3 activity was measured by ELISA, and the proteins related to apoptosis (cyt C, c-IAP1, procaspase 3 and PARP) were assessed by Western blot. Results Compared to treatment with either 0.3 μmol/L imatinib or 20 μmol/L meisoindigo alone, mitochondrial transmembrane potentials declined, soluble cytochrome C (cyt C) released into cytoplasm, procaspase 3 decreased, caspase 3 activity increased significantly, PARP (substrate of caspase 3) was cleavaged and then Annexin V increased when these two drugs were used in combination. Conclusion Meisoindigo interacts synergistically with imatinib to induce apoptosis of K562 cells.