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目的观察茯苓酸对人乳腺癌MDA-MB-231细胞增殖及凋亡的影响,并初步探讨作用机制。方法乳腺癌MDA-MB-231细胞与不同浓度(1、2、5μmol/L)的茯苓酸共孵育,采用CCK-8细胞增殖与活性检测试剂盒检测细胞存活率;流式细胞术Annexin V/PI双染色检测细胞凋亡;Western blotting法检测多聚腺苷二磷酸核糖聚合酶(PARP)及与细胞凋亡相关蛋白的表达。结果茯苓酸能够剂量和时间依赖性地抑制MDA-MB-231细胞的增殖,并可诱导MDA-MB-231细胞凋亡。浓度为1、2、5μmol/L的茯苓酸作用MDA-MB-231细胞48 h后,细胞凋亡率显著增加至25.6%、59.4%、87.2%,明显高于对照组凋亡率(5.4%);经过1、2、5μmol/L茯苓酸分别处理48 h后,实验组MDA-MB-231细胞中凋亡蛋白标志物PARP裂解量升高,且呈剂量依赖性。结论茯苓酸能抑制MDA-MB-231细胞的增殖并诱导其凋亡,其作用机制与激活PARP有关。
Objective To observe the effect of Poria on the proliferation and apoptosis of human breast cancer MDA-MB-231 cells and to explore the mechanism of action. Methods The MDA-MB-231 cells were incubated with Poria cocos under different concentrations (1, 2, 5μmol / L). Cell viability was detected by CCK-8 cell proliferation and activity assay kit. Flow cytometry Annexin V / PI double staining was used to detect apoptosis. Western blotting was used to detect the expression of PARP and apoptosis related proteins. Results Pachyrin acid could inhibit the proliferation of MDA-MB-231 cells in a dose-and time-dependent manner and induce the apoptosis of MDA-MB-231 cells. The apoptosis rate of MDA-MB-231 cells treated with paullinc acid at a concentration of 1,2,5μmol / L for 48 h was significantly increased to 25.6%, 59.4% and 87.2%, which was significantly higher than that of the control group (5.4% ). After treated with 1,2,5 μmol / L of pachyrin acid for 48 h, the cleavage of PARP in MDA-MB-231 cells was increased in a dose-dependent manner. Conclusion Pachyrin can inhibit the proliferation and induce the apoptosis of MDA-MB-231 cells. Its mechanism is related to the activation of PARP.