CAJ | 학술논문

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-pNA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。
목적：：이인원수세포백혈병세포HL-60위례,관찰좌선-이탈수이지순쌍갑광산지( DMDAI-L)대HL-60세포적유도조망작용,초보탐토기작용궤제。방법：통과매해가견광저물DEVD-pNA측정급약전후HL-60세포내적caspase-3매활성；막전위의뢰성결합적형광탐침JC-1표기법관찰급약전후세포선립체막전위(△Ψm)적형광변화。결과：DMDAI-L 1.25,2.5,5,10화20μg·ml-1제량조작용24 h후,HL-60세포내적caspase-3매활성현저상승(P<0.05)；재DMDAI-L작용하,수착농도증가급작용시간연장,HL-60세포내선립체막전위명현강저。결론： DMDAI-L유도HL-60세포조망과정중,기작용궤제가능여재일정제량범위급작용시간내,격활혹조절세포내적caspase-3매활성、강저세포선립체막전위유관。
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-pNA. The fluorescence changes of mito-chondrial membrane potential (△Ψm) in HL-60 cells were investigated with the fluorescent probe JC-1. Results:The caspase-3 activ-ity 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-1 for 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.