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

• 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

書誌事項

タイトル別名

• 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

抄録

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.

収録刊行物

• Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ

  Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ 29 (6), 1082-1086, 2006

  公益社団法人 日本薬学会

キーワード

• <i>Radix Paeoniae Alba</i>
• apoptosis
• HL-60 leukemic cell

詳細情報

• CRID: 1390282679604187008
• NII論文ID: 110005602247
• NII書誌ID: AA10885497
• DOI: 10.1248/bpb.29.1082
• ISSN: 13475215
• ISSN: 09186158
• NDL書誌ID: 7921154
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I7921154
• Web Site: http://www.jstage.jst.go.jp/article/bpb/29/6/29_6_1082/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2007004690
• 本文言語コード: en
• データソース種別:
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  • NDL
  • Crossref
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可