2008 | OriginalPaper | Buchkapitel
Study of Solanine on Mitochondrion in HepG2 Cell
verfasst von : Shiyong Gao, Yubin Ji, Chenfeng Ji, Xiang Zou
Erschienen in: 7th Asian-Pacific Conference on Medical and Biological Engineering
Verlag: Springer Berlin Heidelberg
Aktivieren Sie unsere intelligente Suche, um passende Fachinhalte oder Patente zu finden.
Wählen Sie Textabschnitte aus um mit Künstlicher Intelligenz passenden Patente zu finden. powered by
Markieren Sie Textabschnitte, um KI-gestützt weitere passende Inhalte zu finden. powered by
Objective: To observe the effect of solanine on the membrane potential of mitochondria in HepG
2
cells and [Ca
2+
]
i
in the cells, and to uncover the mechanism by which solanine induces apoptosis.Methods: HepG
2
cells are double stained with AO/EB, and morphological changes of the cells are observed using laser confocal scanning microscopy (LCSM). HepG
2
cells are stained with TMRE, and change in the membrane potential of mitochondria in the cells are observed using LCSM. HepG
2
cells are double stained with Fluo-3/AM, and change of [Ca
2+
]
i
in the cells are observed using LCSM. HepG
2
cells are 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 are observed using LCSM.Results: Cells in treated groups show typical signs of apoptosis. The results of staining with TMRE show that solanine can lower membrane potential; those of staining with Fluo-3/AM show that solanine can increase the concentration of Ca
2+
in tumor cells; and those of double staining with TMRE and Fluo-3/AM show that solanine can lower membrane potential; those of staining with TMRE show that solanine can increase the concentration of Ca
2+
in the cells at the same time as it lowers the membrane potential of mitochondria. Conclusions: 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.