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

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  • Kwon Kang Beom
    Rehabilitation, School of Oriental Medicine, Wonkwang University
  • Kim Eun Kyung
    Department of Physiology, School of Oriental Medicine, Wonkwang University
  • Han Mi Jeong
    Department of Physiology, School of Oriental Medicine, Wonkwang University
  • Shin Byung Cheul
    Rehabilitation, School of Oriental Medicine, Wonkwang University
  • Park Yong Kweon
    Internal Medicine, School of Oriental Medicine, Wonkwang University
  • Kim Kang San
    Internal Medicine, School of Oriental Medicine, Wonkwang University
  • Lee Young Rae
    Department of Biochemistry, Medical School, Chonbuk National University Institute for Healthcare Technology Development, Chonbuk National University
  • Park Jin Woo
    Department of Biochemistry, Medical School, Chonbuk National University Institute for Healthcare Technology Development, Chonbuk National University
  • Park Byung Hyun
    Department of Biochemistry, Medical School, Chonbuk National University Institute for Healthcare Technology Development, Chonbuk National University
  • Ryu Do Gon
    Department of Physiology, School of Oriental Medicine, Wonkwang University

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

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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.

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