SD118-2对人HepG2细胞凋亡影响及机制探讨

The effects and mechanisms of SD118-2 on human HepG2 cells apoptosis

目的观察化合物SD118-2对人HepG2细胞增殖、凋亡及细胞周期的影响。方法取对数生长期人HepG2细胞,分为对照组和给药组。给药组分别给予7 mg/L SD118-2处理12、24和48 h,对照组给予相同浓度DMSO。用MTT法检测细胞增殖率,DAPI荧光染色法观察SD118-2处理后细胞形态,流式细胞仪AnnexinⅤ-FITC/PI双标法检测细胞凋亡率及周期阻滞,用流式细胞仪JC-1染色法检测线粒体膜电位(ΔΨm),Western blot检测凋亡相关蛋白BCL-2、BAX、PARP和C-PARP表达。结果 SD118-2呈时间依赖性抑制人HepG2细胞生长、降低线粒体膜电位、诱导细胞凋亡、阻滞细胞G2期;抗凋亡蛋白BCL-2表达呈时间依赖性减少,促凋亡蛋白BAX、C-PARP表达呈时间依赖性增加;SD118-2对正常肝脏细胞增殖几乎无影响。结论化合物SD118-2具有诱导人HepG2细胞凋亡的作用,并能使细胞周期进程发生变化。

Objective To study the effects of SD118-2 on human HepG2 cells proliferation, cell cycle and cell ap- optosis. Methods The proliferation of cells was detected by MTI＂ assay. The modality of cells was detected by the fluorescence microscopy with DAPI staining. The cell apoptosis, cell cycle and mitochondrial membrane potential were detected by the flow cytometer. The apoptosis associated with BCL-2, BAX, PARP, C-PARP was detected by Western blot. Results membrane potential and BCL-2 and up-regulated SDl18-2 inhibited the proliferation of human HepG2 cells, decreased the mitochondrial induced cell apoptosis, blocked the cells in G2 stage, down-regulated the expression of expression of BAX, C-PARP at a time-dependent manner. At the same time, the effects of SDl18-2 on normal human liver cell apoptosis and block the cell was very weak. Conclusions SD118-2 can inhibit the cell proliferation, induce in G2 stage of HepG2.