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目的:本试验旨在研究白桦脂酸诱导乳腺癌细胞凋亡的机制。方法:采用细胞凋亡、线粒体膜电位和Caspsase 3活性检测的方法。结果:12 h与6 h白桦脂酸从40μmol/L(0.36±0.03,0.65±0.04)开始可显著降低乳腺癌细胞MCF-7存活率;白桦脂酸使细胞凋亡率(20μmol/L:0.29±0.09,40μmol/L:0.58±0.10,60μmol/L:0.78±0.13)明显高于其空白对照组(0.03±0.01)。白桦脂酸组细胞线粒体膜电位(20μmol/L:40.59±5.49,40μmol/L:10.90±2.59,60μmol/L:1.49±0.10)明显低于其空白对照组(80.34±3.45)。在白桦脂酸40μmol/L和60μmol/L作用下,乳腺癌细胞核均发生了变化,发生明显的聚缩。白桦脂酸各组Caspase 3活性(20μmol/L:0.34±0.11,40μmol/L:0.63±0.17,60μmol/L:0.70±0.07)明显高于其空白对照组(0.17±0.03)。结论:白桦脂酸可诱导乳腺癌细胞凋亡,降低线粒体膜电位,激活调节下游凋亡相关蛋白caspase-3的活性。
Aims: The aim of this study was to investigate the mechanism of betulinic acid-induced apoptosis in breast cancer cells. Methods: Apoptosis, mitochondrial membrane potential and Caspsase 3 activity were measured. RESULTS: Betulinic acid at 12 h and 6 h significantly reduced the survival rate of MCF-7 breast cancer cells from 40 μmol / L (0.36 ± 0.03,0.65 ± 0.04). Betulinic acid induced apoptosis (20 μmol / L: 0.29 ± 0.09,40μmol / L: 0.58 ± 0.10,60μmol / L: 0.78 ± 0.13) was significantly higher than that of the blank control group (0.03 ± 0.01). The betulinic acid group mitochondrial membrane potential (20μmol / L: 40.59 ± 5.49,40μmol / L: 10.90 ± 2.59,60μmol / L: 1.49 ± 0.10) was significantly lower than the blank control group (80.34 ± 3.45). In betulinic acid 40μmol / L and 60μmol / L under the action of breast cancer cell nuclei have changed, the occurrence of significant polycondensation. The activity of caspase 3 (20μmol / L: 0.34 ± 0.11,40μmol / L: 0.63 ± 0.17,60μmol / L: 0.70 ± 0.07) in each group of betulinic acid was significantly higher than that of the blank control group (0.17 ± 0.03). CONCLUSION: Betulinic acid can induce breast cancer cell apoptosis, decrease mitochondrial membrane potential and activate and regulate the activity of downstream apoptosis-related protein caspase-3.