中文摘要：

瞄准：在 HepG (2 ) 房间在线粒体的膜电位上观察茄硷的效果，并且揭开并且[Ca (2+)] 在房间的(i) 茄硷由导致 apoptosis 的机制。方法：HepG (2 ) 房间是双的与 AO/EB 染色了，并且房间的词法变化被观察使用激光共焦的扫描显微镜学(LCSM ) 。HepG (2 ) 房间与 TMRE 被染色，并且在在房间的线粒体的膜电位的变化用 LCSM 被观察。HepG (2 ) 房间是双的与 Fluo-3/AM，和变化染色了[Ca (2+)] 在房间的(i) 用 LCSM 被观察。HepG (2 ) 房间是双的染色了与 TMRE 和 Fluo-3/AM，和两个在线粒体和的膜电位的变化[Ca (2+)] 在房间的(i) 用 LCSM 被观察。结果：在对待的组的房间显示出 apoptosis 的典型符号。与 TMRE 染色显示出那茄硷能更低的膜电位；与 Fluo-3/AM 染色证明茄硷能在肿瘤房间增加 Ca (2+) 的集中；并且那些两倍与 TMRE 和 Fluo-3/AM 染色证明当它降低了线粒体的膜电位，茄硷能在一样的时间在房间增加 Ca (2+) 的集中。结论：茄硷由降低膜电位在膜开创磅隧道，导致 Ca (2+) 在它的集中坡度下面被搬运，它接着在房间导致 Ca (2+) 的集中的上升，打开为 apoptosis 的机制。

英文摘要：

AIM： To observe the effect of solanine on the membrane potential of mitochondria in HepG2 cells and [Ca^2＋]i in the cells, and to uncover the mechanism by which solanine induces apoptosis.METHODS： HepG2 cells were double stained with AO/EB, and morphological changes of the cells were observed using laser confocal scanning microscopy （LCSM）. HepG2 cells were stained with TMRE, and change in the membrane potential of mitochondria in the cells were observed using LCSM. HepG2 cells were double stained with Fluo-3/AM, and change of [Ca^2＋]i in the cells were observed using LCSM. HepG2 cells were double stained with TMRE and Fluo-3/AM, and both the change in membrane potential of mitochondria and that of [Ca^2＋]i in the cells were observed using LCSM.RESULTS： Cells in treated groups showed typical signs of apoptosis. Staining with TMRE showed that solanine could lower membrane potential; staining with Fluo-3/AM showed that solanine could increase the concentration of Ca^2＋ in tumor cells; and those of double staining with TMRE and Fluo-3/AM showed that solanine could increase the concentration of Ca^2＋ in the cells at the same time as it lowered the membrane potential of mitochondria.CONCLUSION： Solanine opens up the PT channels in the membrane by lowering the membrane potential, leading to Ca^2＋ being transported down its concentration gradient, which in turn leads to the rise of the concentration of Ca^2＋ in the cell, turning on the mechanism for apoptosis.