Zhang Aifeng, Sheng Yuqing, Zou Mingchang
The Fourth Pepole's Hospital of Zhenjiang, Zhenjiang, 212002, China.
The First Pepole's Hospital of Zhenjiang, Zhenjiang, 212002, China.
Biomed Pharmacother. 2017 Mar;87:110-117. doi: 10.1016/j.biopha.2016.12.088. Epub 2016 Dec 31.
Previous studies have demonstrated that Alisol B has inhibitory activity in cancer cells. However, the exact mechanism through which inhibition is achieved is still poorly understood. In the present study, the authors examined the effects of Alisol B in human breast cancer cells. Alisol B showed significant anticancer activity in MDA-MB-231 cells. The results demonstrated that the cytotoxicity induced by Alisol B was mediated by induction of apoptosis, decrease in mitochondrial membrane potential, cell cycle arrest, activation of caspases and accumulation of ROS (reactive oxygen species) level. Interestingly, pretreatment of cells with the general caspase inhibitor z-VAD-FMK significantly prevented Alisol B-induced apoptosis. Furthermore, western blot analysis revealed the upregulation of p-p38 and downregulation of p-AKT, p-p65 and p-mTOR. Taken together, the above results suggest that Alisol B suppresses the growth of MDA-MB-231 cells mainly through induction of apoptosis; this outcome may represent the major mechanism of Alisol B-mediated apoptosis.
先前的研究表明，泽泻醇B在癌细胞中具有抑制活性。然而，实现抑制的确切机制仍知之甚少。在本研究中，作者研究了泽泻醇B对人乳腺癌细胞的影响。泽泻醇B在MDA-MB-231细胞中显示出显著的抗癌活性。结果表明，泽泻醇B诱导的细胞毒性是通过诱导凋亡、线粒体膜电位降低、细胞周期停滞、半胱天冬酶激活和活性氧（ROS）水平积累介导的。有趣的是，用通用的半胱天冬酶抑制剂z-VAD-FMK预处理细胞可显著预防泽泻醇B诱导的凋亡。此外，蛋白质印迹分析显示p-p38上调，p-AKT、p-p65和p-mTOR下调。综上所述，上述结果表明，泽泻醇B主要通过诱导凋亡抑制MDA-MB-231细胞的生长；这一结果可能代表了泽泻醇B介导凋亡的主要机制。
