摘要
目的:观察太白楤木总皂苷对白血病K562、U937细胞增殖的抑制作用,并探讨其诱导K562细胞早期凋亡的作用机制。方法:体外培养人白血病K562、U937细胞株,按照处理因素的不同分为空白对照组和药物处理组,MTT法检测太白楤木总皂苷对白血病细胞增殖的抑制作用;倒置显微镜下观察K562细胞形态学变化;流式细胞术检测其对K562细胞线粒体膜电位的影响;免疫细胞化学法检测太白楤木总皂苷作用后抗凋亡相关基因BCL-2、BAX在K562细胞中的表达。结果:太白楤木总皂苷对两种白血病细胞株增殖均有较强的抑制作用,呈现时间及剂量依赖关系。倒置显微镜下观察结果与MTT实验结果一致。太白楤木总皂苷能够诱导K562细胞线粒体膜电位下降。经太白楤木总皂苷作用后,BCL-2基因蛋白在K562细胞中的表达减弱,BAX在K562细胞中的表达增强。结论:太白楤木总皂苷能抑制两种白血病细胞株的增殖,其机制可能与诱导白血病细胞早期凋亡相关。
Objective:To investigate the effect of total saponin of Aralia Taibaiensis on the leukemia cells and explore the mecha- nisms of early apoptosis. Methods:The leukemia cells lines K562 and U937 were cultured in vitro and divided into 2 groups:control group and treatment group. The proliferation inhibition of leukemia cells was measured by MTT assay. K562 cells morphological chan- ges were observed under the reverse microscope;Flow cytometry (FCM) was used to detect the influence of total saponin of Aralia Taibaiensis on changes of mitochondrial membrane potential in K562 cells. The expression of protein BCL-2 and BAX in /(562 cells was investigated by immunohistochemistry. Resuhs:The total saponin of Aralia Taibaiensis had significant inhibitory effects on K562 and U937 cell lines, and the inhibitory effects on these two cells lines presented time-dependent and dose-dependent manner. The results by inverted microscope were consistent with that of the MTF assay. FCM analysis showed that total saponin of Aralia Taibaiensis could induce mitochondrial membrane potential of K562 cells. Compared with control group, the expression of BCL-2 in treatment group was down-regulated, the expression of BAX was significantly up-regulated. Conclusion : The total saponin of Aralia Taibaiensis can inhibit two kinds of leukemia cells lines in vitro,and the mechanism may be related to promoting the early apoptosis of K562 cells.
出处
《中药材》
CAS
CSCD
北大核心
2013年第4期604-607,共4页
Journal of Chinese Medicinal Materials
基金
陕西省教育厅资助项目(2013JK0826)
咸阳市科技局资助项目(2012K16-01-5)
关键词
太白楤木总皂苷
凋亡
增殖抑制
线粒体膜电位
BCL-2
BAX
Total saponin of Aralia Taibaiensis
Apoptosis
Proliferation inhibition
Mitochondrial membrane potential
BCL-2
BAX