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目的探讨金雀异黄素对结肠癌细胞HCT-116的细胞增殖和凋亡的影响及其可能的机制。方法不同浓度金雀异黄素处理HCT-116细胞,MTT法测定细胞存活率,流式细胞仪检测细胞周期、细胞凋亡、细胞内活性氧(ROS)水平和线粒体膜电位的变化,并用透射电镜观察细胞的超微结构。结果金雀异黄素呈剂量和时间依赖性地抑制细胞增殖。0~100μmol/L的金雀异黄素处理细胞24 h后引起G2/M期阻滞,凋亡峰Sub-G1所占细胞比例从(1.63±0.44)%增至(8.33±1.51)%(P<0.01),早期凋亡细胞从(1.93±0.32)%增至(7.25±0.86)%(P<0.01)。透射电镜下细胞出现凋亡特征性改变。100μmol/L金雀异黄素处理后细胞内ROS水平在2 h时增至处理前的1.81倍,(15.53±1.55)%vs(8.57±0.35)%,P<0.01,细胞线粒体膜电位在1 h时迅速下降了87.8%,(0.82±0.02)%vs(6.70±0.21)%,P<0.01。结论金雀异黄素抑制结肠癌细胞株HCT-116的细胞增殖,引起G2/M期细胞阻滞并促进细胞凋亡,可能与升高细胞内ROS水平,降低线粒体膜电位有关。
Objective To investigate the effects of genistein on cell proliferation and apoptosis of human colon cancer cell line HCT-116 and its possible mechanism. Methods HCT-116 cells were treated with genistein at different concentrations. Cell viability was measured by MTT assay. Cell cycle, apoptosis, intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were measured by flow cytometry. Electron microscopy cell ultrastructure. Results Genistein inhibited cell proliferation in a dose- and time-dependent manner. The cells treated with genistein at 0-100 micromol / L for 24 h resulted in G2 / M arrest and the percentage of Sub-G1 cells increased from (1.63 ± 0.44)% to (8.33 ± 1.51)% ( P <0.01). The number of apoptotic cells in the early stage increased from (1.93 ± 0.32)% to (7.25 ± 0.86)% (P <0.01). Cell apoptosis under transmission electron microscope characteristic changes. After treated with 100μmol / L genistein, the intracellular ROS level increased to 1.81 times, (15.53 ± 1.55)% vs (8.57 ± 0.35)%, P <0.01 h decreased rapidly by 87.8%, (0.82 ± 0.02)% vs (6.70 ± 0.21)%, P <0.01. Conclusions Genistein can inhibit cell proliferation of human colon cancer cell line HCT-116, induce cell arrest in G2 / M phase and promote cell apoptosis, which may be related to the increase of intracellular ROS level and mitochondrial membrane potential.