Chen Jung-Chou, Lu Kung-Wen, Lee Jau-Hong, Yeh Chin-Chung, Chung Jing-Gung
Chinese Medical Research Institute, China Medical University, Taichung, Taiwan, ROC.
Anticancer Res. 2006 Nov-Dec;26(6B):4313-26.
The effects of the gypenosides (Gyp), a component of Gynostemma pentaphyllum Makino, on the cell viability, cell cycle and induction of apoptosis were investigated in human colon cancer colo 205 cells. Gyp was cytotoxic to colo 205 cells with an IC50 of 113.5 microg/ml. The decreasing number of viable cells appeared to be due to the induction of cell cycle arrest and apoptotic cell death, since Gyp induced morphological changes and internucleosomal DNA fragmentation and increased the sub-G1 group. The production of reactive oxygen species and Ca2+ and the depolarization of mitochondrial membrane potential were observed, dose- and time-dependently, after treatment with various concentrations of Gyp. Gyp treatment also gradually decreased the expression of the anti-apoptotic proteins Bcl-2 and Bcl-xl, but increased the expression of the pro-apoptotic protein Bax. Gyp increased the levels of p53 and promoted the release of cytochrome c and the activation of caspase-3 before leading to apoptosis. These results provide information towards an understanding of the mechanisms by which Gyp induces cell cycle arrest and apoptosis in human colon cancer cells.
研究了绞股蓝主要成分绞股蓝皂苷（Gyp）对人结肠癌colo 205细胞的细胞活力、细胞周期及凋亡诱导作用。Gyp对colo 205细胞具有细胞毒性，IC50为113.5微克/毫升。活细胞数量减少似乎是由于细胞周期阻滞和凋亡性细胞死亡的诱导，因为Gyp诱导了形态学变化和核小体间DNA片段化，并增加了亚G1期细胞群。用不同浓度的Gyp处理后，观察到活性氧、Ca2+的产生以及线粒体膜电位的去极化呈剂量和时间依赖性。Gyp处理还逐渐降低了抗凋亡蛋白Bcl-2和Bcl-xl的表达，但增加了促凋亡蛋白Bax 的表达。在导致凋亡之前，Gyp增加了p53的水平，促进了细胞色素 c的释放和caspase-3的激活。这些结果为理解Gyp诱导人结肠癌细胞周期阻滞和凋亡的机制提供了信息。
