Abstract
In the present study we have investigated whether butein could induce apoptosis in human leukaemic HL-60 cells. The treatment of HL-60 cells with butein induced apoptotic cell death as determined by morphological and biochemical changes. Apoptotic DNA fragments in the butein-treated HL-60 cells were increased gradually as determined by flow cytometric analysis. The caspase-3 activity was increased during butein-induced apoptosis. However, caspase-3 inhibitor abrogated the butein-induced DNA fragmentation. Furthermore, the treatment of HL-60 cells with butein decreased the expression of Bcl-2 protein, but increased the expression of Bax protein. These results suggest that butein-induced apoptosis is mediated through the activation of caspase-3 and it is associated with changed expression of Bcl-2 and Bax proteins.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / drug effects*
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Caspase 3
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Caspases / metabolism*
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Cell Survival / drug effects
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Chalcone / analogs & derivatives*
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Chalcone / pharmacology*
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Chalcones
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DNA Fragmentation / drug effects
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Dose-Response Relationship, Drug
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Electrophoresis, Agar Gel
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Enzyme Activation
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Enzyme Precursors
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Flow Cytometry
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HL-60 Cells
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HeLa Cells
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Humans
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K562 Cells
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Phosphodiesterase Inhibitors / pharmacology*
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Ploidies
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Proto-Oncogene Proteins / metabolism*
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Proto-Oncogene Proteins c-bcl-2 / metabolism*
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Tumor Cells, Cultured
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U937 Cells
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bcl-2-Associated X Protein
Substances
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BAX protein, human
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Chalcones
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Enzyme Precursors
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Phosphodiesterase Inhibitors
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2
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bcl-2-Associated X Protein
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butein
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Chalcone
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CASP3 protein, human
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Caspase 3
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Caspases