太白楤木总皂苷对K562细胞增殖抑制及其作用机制的研究  

Effects and Mechanisms of Total Saponin of Aralia Taibaiensis on Human Leukemia Cell Line K562

作　　者：范妤[1] 郭东艳[1] 宋强 李涛[1] 

机构地区：[1]陕西中医学院,咸阳712046 [2]陕西省核工业215医院,咸阳712046

出　　处：《医学研究杂志》2013年第7期92-94,共3页Journal of Medical Research

基　　金：陕西省教育厅基金资助项目(2013JK0826);咸阳市科技局基金资助项目(2012K16-01-5)

摘　　要：目的以人慢性髓系白血病细胞株K562细胞为模型,研究太白楤木的体外抗肿瘤活性及其作用机制。方法MTT法检测太白楤木总皂苷对K562细胞的增殖抑制作用;单细胞凝胶电泳检测K562细胞DNA损伤;流式细胞术检测K562细胞细胞周期的改变。结果太白楤木总皂苷对K562细胞增殖具有抑制作用,并呈时间-剂量依赖性;能显著诱导K562细胞DNA损伤;促进凋亡的发生;细胞周期阻滞于S期。结论太白楤木总皂苷能抑制K562细胞的增殖,诱导凋亡发生,其机制可能与通过诱导K562细胞DNA损伤来改变细胞周期时相的分布有关。Objective To study anti - tumor activity in vitro and related mechanism of Total saponin of Aralia Taibaiensis（SAT） on Human Leukemia Cell Lline K562. Methods The proliferation inhibition was measured by MTT assay. DNA injury was evaluated by single cell gel electrophoresis Assay （ SCGE）. Changes of cell cycle were detected using flow cytometr. Result SAT inhibited K562 cells proliferation on a time - and dose - dependent manner. SAT induced DNA injury of K562 significantly. SAT promoted the occurrence of apoptosis. The cell cycle was arrested in S phase after SAT treatment. Conclusion SAT inhibited K562 cells proliferation and induced cell apoptosis on a dose - dependent manner. The mechanism may be related the induction of K562 cell DNA damage and the change of the distribution of cell cycle phase.

关 键 词：太白楤木总皂苷 K562细胞 DNA损伤 周期阻滞 

分 类 号：R971.1[医药卫生—药品]