左旋-二脱水伊地醇双甲磺酸酯诱导HL-60细胞凋亡机制的研究  

Study on Mechanism of HL-60 Cell Apoptosis Induced by DMDAI-L

作　　者：曹斌[1] 刘元[1] 曾春[2] 杨小叶[2] 杨斌[2] 

机构地区：[1]广西中医药研究院,南宁530022 [2]广西医科大学药学院

出　　处：《中国药师》2015年第2期186-189,共4页China Pharmacist

基　　金：广西自然科学基金项目应用基础研究专项基金(编号:桂科基0991013)

摘　　要：目的:以人原髓细胞白血病细胞HL-60为例,观察左旋-二脱水伊地醇双甲磺酸酯(DMDAI-L)对HL-60细胞的诱导凋亡作用,初步探讨其作用机制。方法:通过酶解可见光底物DEVD-p NA测定给药前后HL-60细胞内的caspase-3酶活性;膜电位依赖性结合的荧光探针JC-1标记法观察给药前后细胞线粒体膜电位(△Ψm)的荧光变化。结果:DMDAI-L 1.25,2.5,5,10和20μg·ml-1剂量组作用24 h后,HL-60细胞内的caspase-3酶活性显著上升(P<0.05);在DMDAI-L作用下,随着浓度增加及作用时间延长,HL-60细胞内线粒体膜电位明显降低。结论:DMDAI-L诱导HL-60细胞凋亡过程中,其作用机制可能与在一定剂量范围及作用时间内,激活或调节细胞内的caspase-3酶活性、降低细胞线粒体膜电位有关。Objective： To explore the effect and mechanism of DMDAI-L in inducing the HL-60 cells apoptosis. Methods：Caspase-3 activity in HL-60 cells was measured with the enzymatic visible substrate DEVD-p NA. The fluorescence changes of mitochondrial membrane potential（ △Ψm） in HL-60 cells were investigated with the fluorescent probe JC-1. Results： The caspase-3 activity was significantly increased in HL-60 cells after the DMDAI-L treatment at the concentration of 1. 25,2. 5,5,10 and 20μg·ml- 1for 24h（ P 0. 05）. DMDAI-L could significantly reduce the mitochondrial membrane potential in HL-60 cells. Conclusion： The mechanism of DMDAI-L in inducing HL-60 cells apoptosis may involve the activation or regulation of caspase-3 activity as well as the reduction of mitochondrial membrane potential in HL-60 cells within certain concentration and time range.

关 键 词：左旋-二脱水伊地醇双甲磺酸酯 HL-60细胞 细胞凋亡 Caspase-3酶活性 

分 类 号：R965.1[医药卫生—药理学]