CAJ | 학술논문

目的对β-榄香烯哌嗪衍生物DX2体外抑制人肝癌HepG2细胞增殖作用及其机制进行研究. 方法采用MTT法测定细胞存活情况;采用倒置显微镜及吖啶橙染色观察细胞形态学变化;用流式细胞仪检测凋亡细胞比率及线粒体膜电位变化. 用免疫印迹法分析DX2对细胞凋亡线粒体通路蛋白水平的影响. 结果 DX2可明显抑制HepG2细胞增殖,诱导细胞出现凋亡小体,增加凋亡细胞比率. 免疫印迹结果显示,35μmol/L DX2作用细胞后呈时间依赖性地降低HepG2细胞的线粒体膜电位,上调Bax/Bcl-2的比值,促进细胞色素c向胞浆释放,激活胱天蛋白酶(caspase)-9及其下游caspase-3,降解caspase-3底物ICAD. 结论 DX2可诱导HepG2细胞凋亡,其机制为激活细胞凋亡线粒体途径.
목적 대β-람향희고진연생물DX2체외억제인간암HepG2세포증식작용급기궤제진행연구. 방법 채용MTT법측정세포존활정황;채용도치현미경급아정등염색관찰세포형태학변화;용류식세포의검측조망세포비솔급선립체막전위변화. 용면역인적법분석DX2대세포조망선립체통로단백수평적영향. 결과 DX2가명현억제HepG2세포증식,유도세포출현조망소체,증가조망세포비솔. 면역인적결과현시,35μmol/L DX2작용세포후정시간의뢰성지강저HepG2세포적선립체막전위,상조Bax/Bcl-2적비치,촉진세포색소c향포장석방,격활광천단백매(caspase)-9급기하유caspase-3,강해caspase-3저물ICAD. 결론 DX2가유도HepG2세포조망,기궤제위격활세포조망선립체도경.
Objective To study the antiproliferative effect of DX2, a piperazine derivate of β-elemene, on human hepatoma HepG2 cells. Methods Cell viability was measured by MTT method. Morphological changes were observed by phase contrast microscopy and acridine orange staining. Apoptotic cell ratio was measured by flow cytometric analysis. Protein level was detected by Western blot analysis. Results DX2 Induced apoptotic morphological changes in HepG2 cells and increased the ratio of apoptotic cells. Treatment of HepG2 cells with DX2 increased the Bax/Bcl-2 ratio, induced the activation of caspase-9 and caspase-3 and caused the degradation of ICAD which was the substrate of capase-3. Conclusion DX2 Induces HepG2 cell death via activation of intrinsic mitochondrial pathway.