Induction of Apoptosis by Radix Paeoniae Alba Extract through Cytochrome c Release and the Activations of Caspase-9 and Caspase-3 in HL-60 Cells

Radix Paeoniae Alba has been used as a constituent of herbal medicine prescriptions for the treatment of inflammation, cancer, and other diseases. The aim of this study was to investigate the mechanism of Radix Paeoniae Alba extract (RPAE)-induced apoptosis in HL-60 leukemic cells. We observed that...

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Bibliographic Details
Published in:Biological & pharmaceutical bulletin 2006, Vol.29(6), pp.1082-1086
Main Authors: Kwon, Kang Beom, Kim, Eun Kyung, Han, Mi Jeong, Shin, Byung Cheul, Park, Yong Kweon, Kim, Kang San, Lee, Young Rae, Park, Jin Woo, Park, Byung Hyun, Ryu, Do Gon
Format: Article
Language:English
Subjects:
apoptosis
Apoptosis - drug effects
Blotting, Western
Caspase 3 - metabolism
Caspase 9 - metabolism
Caspase Inhibitors
Cell Survival - drug effects
Cytochromes c - metabolism
Cytosol - drug effects
Cytosol - metabolism
DNA Fragmentation - drug effects
Dose-Response Relationship, Drug
Electrophoresis, Agar Gel
Enzyme Activation
Enzyme Inhibitors - pharmacology
HL-60 Cells
HL-60 leukemic cell
Humans
Mitochondria - drug effects
Mitochondria - metabolism
Paeonia - chemistry
Plant Extracts - isolation & purification
Plant Extracts - pharmacology
Poly(ADP-ribose) Polymerases - metabolism
Radix Paeoniae Alba
Time Factors
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Summary:Radix Paeoniae Alba has been used as a constituent of herbal medicine prescriptions for the treatment of inflammation, cancer, and other diseases. The aim of this study was to investigate the mechanism of Radix Paeoniae Alba extract (RPAE)-induced apoptosis in HL-60 leukemic cells. We observed that RPAE induced apoptotic changes in a dose-dependent manner, which was confirmed by DNA fragmentation and poly-(ADP-ribose) polymerase (PARP) cleavage. We also found release of cytochrome c from mitochondria to the cytosol in RPAE-treated HL-60 cells. The caspases, caspase-9 and -3, but not caspase-8, were found to be activated in response to RPAE treatment, and the caspase-3 inhibitor, Ac-DEVD-CHO, and the caspase-9 inhibitor, z-LEHD-FMK, but not the caspase-8 inhibitor, z-IETD-FMK, attenuated RPAE-induced DNA fragmentation and PARP cleavage. These results suggest that RPAE-induced apoptosis is stimulated by the release of cytochrome c to the cytosol, by procaspase-9 processing, and via a caspase-3 dependent mechanism.
ISSN:0918-6158
1347-5215
DOI:10.1248/bpb.29.1082