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Chromomycin A(2) induces apoptosis of HepG2 cells in vitro / 南方医科大学学报
Article em Zh | WPRIM | ID: wpr-329269
Biblioteca responsável: WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To study the effect of chromomycin A(2) in inducing apoptosis of HepG2 cells and explore the molecular mechanism.</p><p><b>METHODS</b>HepG2, MCF-7, A549, and 7901 cells were exposed to chromomycin A(2) and the changes in the cell viability were detected using MTT assay. The changes in the chromatins were observed with laser scanning confocal microscope after incubation of the cells with chromomycin A(2) (60 nmol/L) for 24 h. The changes in cell morphology were examined with a phase-contrast microscope, and the apoptotic cell populations, fluorescent intensity of reactive oxygen species (ROS) and mitochondrial membrane potential were determined using flow cytometry.</p><p><b>RESULTS</b>Chromomycin A(2) significantly inhibited the proliferation of the cells in a time- and dose-dependent manner, and caused changes in the cell morphology and cell apoptosis. Exposure of the cells to chromomycin A(2) resulted in chromatin condensation, ROS generation, and reduction of the mitochondrial membrane potential.</p><p><b>CONCLUSION</b>Increased ROS and mitochondria damage may importantly contribute to chromomycin A(2)-induced apoptosis in HepG2 cells.</p>
Assuntos
Texto completo: 1 Base de dados: WPRIM Assunto principal: Patologia / Farmacologia / Sobrevivência Celular / Espécies Reativas de Oxigênio / Apoptose / Plicamicina / Potencial da Membrana Mitocondrial / Células Hep G2 / Metabolismo / Mitocôndrias Limite: Humans Idioma: Zh Revista: Journal of Southern Medical University Ano de publicação: 2014 Tipo de documento: Article
Texto completo: 1 Base de dados: WPRIM Assunto principal: Patologia / Farmacologia / Sobrevivência Celular / Espécies Reativas de Oxigênio / Apoptose / Plicamicina / Potencial da Membrana Mitocondrial / Células Hep G2 / Metabolismo / Mitocôndrias Limite: Humans Idioma: Zh Revista: Journal of Southern Medical University Ano de publicação: 2014 Tipo de documento: Article