Baicalein induced in vitro apoptosis undergo caspases activity in human promyelocytic leukemia HL-60 cells

In this study, we evaluated the potential apoptosis effects of baicalein on human promyelocytic leukemia HL-60 cells in vitro. Apoptosis induction, cell viability, morphology and caspase-3 activity were then performed to determine by flow cytometric assay, DNA gel electrophoresis, anti-ADP-ribose st...

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Bibliographic Details
Published in:Food and chemical toxicology 2004, Vol.42 (1), p.37-43
Main Authors: LI, Y. C, TYAN, Y. S, KUO, H. M, CHANG, W. C, HSIA, T. C, CHUNG, J. G
Format: Article
Language:English
Subjects:
Amino Acid Chloromethyl Ketones - pharmacology
Antibodies, Monoclonal
Antineoplastic agents
Antioxidants - pharmacology
Apoptosis - drug effects
Biological and medical sciences
Caspase Inhibitors
Caspases - biosynthesis
Cell Cycle - drug effects
Cell Survival - drug effects
Chemotherapy
DNA Fragmentation - drug effects
Enzyme Inhibitors - pharmacology
Flavanones
Flavonoids - pharmacology
Flow Cytometry
HL-60 Cells
Humans
Indicators and Reagents
Medical sciences
Pharmacology. Drug treatments
Poly(ADP-ribose) Polymerases - metabolism
Trypan Blue
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Summary:In this study, we evaluated the potential apoptosis effects of baicalein on human promyelocytic leukemia HL-60 cells in vitro. Apoptosis induction, cell viability, morphology and caspase-3 activity were then performed to determine by flow cytometric assay, DNA gel electrophoresis, anti-ADP-ribose stain and determination of caspase-3 activity. There is a significant difference in cell death of HL-60 cells that was detected between baicalein-treated and untreated groups. Furthermore, there was a further significant increase in apoptosis induction when cells were treated with baicalein compared to without baicalein treated groups. Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed baicalein induced apoptosis in HL-60 cells. Baicalein also promoted caspase-3 activity then leading to cleavage of poly-ADP-ribose polymerase finally leading to DNA fragmentation occurrence. Furthermore, the baicalein-induced apoptosis was markedly blocked by the broad-spectrum caspase inhibitor, z-VAD-fmk. Taken together, these results suggest that treatment of human leukemia HL-60 cells with baicalein induced apoptosis through activation of caspase-3 activity.
ISSN:0278-6915
1873-6351
DOI:10.1016/j.fct.2003.08.014