摘要
目的 研究番荔枝内酯 (squamocin)诱导白血病细胞凋亡的机理。方法 DNA凝胶电泳法、荧光染色等检测细胞凋亡。试剂盒检测caspase 3的活性。Westernblot法检测PARP和caspase 3的剪切片断和磷酸化的SAPK JNK量的变化。结果 Squamocin处理HL 6 0细胞后 ,导致染色质浓缩、片断化 ,DNA梯形条带出现 ,完整PARP的 116ku条带逐渐减少 ,而 85ku的片断逐渐增加 ,caspase 3酶的活性也增加。Caspase 3的特异性抑制剂DEVD CHO预处理HL 6 0细胞 ,可阻止squamocin诱导的DNA片断化、PARP的剪切和细胞死亡。Squamocin激活HL 6 0细胞中SAPK JNK。结论 Squamocin诱导HL 6 0细胞凋亡依赖caspase 3途径的激活 ,squamocin激活caspase 3可能与SAPK
AIM To investigate the mechanism of apoptosis of HL60 cells induced by the annonaceous acetogenin, squamocin. METHODS Induction of apoptosis was determined through Hoechst33258 dye staining and DNA agarose gel electrophoresis. Expression of the proteins was detected using Western blot analysis. Caspase 3 activity was detected using caspase 3 kit. RESULTS Treatment of HL 60 cells with squamocin resulted in extensive nuclear condensation, DNA fragmentation, cleavage of the death substrate poly(ADP ribose) polymerase (PARP) and induction of caspase 3 activity. Pretreatment of HL 60 cells with caspase 3 specific inhibitor DEVD CHO prevented squamocin induced DNA fragmentation, PARP cleavage and cell death. Stress activated protein kinase (SAPK/JNK) was activated after treatment with squamocin in HL 60 cells. CONCLUSION These results suggest that apoptosis of HL 60 cells induced by squamocin require caspase 3 activation, and could be related to SAPK activation.
出处
《药学学报》
CAS
CSCD
北大核心
2001年第7期498-501,共4页
Acta Pharmaceutica Sinica
基金
中山医科大学"2 11工程"重点学科项目 (980 69)
