白花丹醌诱导人白血病细胞-NB4凋亡的实验研究

Plumbagin Induces Apoptosis of Human Leukemia Cell-NB4

目的:探讨白花丹醌诱导人白血病细胞-NB4的凋亡途径。方法:取白花丹醌终浓度10μmol/L作用于人白血病细胞-NB4不同时间,比色法测定半胱氨酸天冬氨酸蛋白酶-3,-8,-9(caspase-3,-8,-9)的活性;westenblot显示死亡受体凋亡途径中重要蛋白:caspase-8和Bid的裂解;流式分析caspase酶抑制剂作用下白花丹醌诱导NB4细胞凋亡的改变。结果:白花丹醌通过激活包括caspase-8和Bid在内的caspase依赖途径诱导NB4细胞凋亡。结论:caspase-8是白花丹醌抗白血病作用的重要环节。死亡受体途径可能在白花丹醌诱导白血病细胞凋亡过程中具有重要作用。

Objective： To explore the apoptosis pathway involved in plumbagin-treated human leukemia cells-NB4. Methods： NB4 cells were cultured with plnmbagin at final concentration of 10 μmol/L for different times. Cas- pase-3,-8,-9 activity was confirmed by colorimetric assay, cleavage of caspase-8 and Bid which were key posi- tion in the death-receptor pathway of apoptosis were presented by western blot,and apoptosis induced by plumba- gin under caspase inhibitors was measured by flow cytometry. Results： Plumbagin-induced apoptosis was a cas- pase-mediated pathway involving activation of caspase-8 and Bid. Conclusion： Caspase-8 is involved in the plumbagin effect, and death-receptor pathway of apoptosis will be an important event in the plumbagin-induced apoptosis process of leukemia cells.