Broussochalcone B from Broussonetia papyrifera Induce Apoptosis via Activation of a Caspase Cascade and Reactive Oxygen Species Production in Human HepG2 cells

꾸지나무 유래 화합물 Broussochalcone B의 HepG2 간암세포의 세포사멸에 미치는 영향

  • Park, Jin Ryang (Department of Life Science, Seonam University) ;
  • Ryu, Hyung Won (Natural Medicine Research Center, Korea Research Institute of Bioscience & Biotechnology) ;
  • Cho, Byoung Ok (Department of Health Care & Management, Jeonju University)
  • 박진량 (서남대학교 생명과학과) ;
  • 류형원 (한국생명공학연구원 천연물의약연구센터) ;
  • 조병옥 (전주대학교 보건관리학과)
  • Received : 2017.11.28
  • Accepted : 2017.12.15
  • Published : 2017.12.29

Abstract

The aim of this study was to investigate the mechanisms underlying apoptosis induced by a broussochalcone B (BCB) from Broussonetia papyrifera in HepG2 cells. The results showed that BCB treatment for 24 hr significantly inhibited cell viability in a dose-dependent manner, and induced apoptosis in HepG2 cells. More so, BCB treatment triggered the cleavage of caspase-8, -9, -3, poly (ADP-ribose) polymerase (PARP), increase of Bax level, and decrease of Bcl-2 expression. A general caspase inhibitor (z-VAD-fmk) blocked BCB-induced cell death. Furthermore, BCB treatment caused reactive oxygen species (ROS) production in a dose-dependent manner. In addition, an antioxidant N-acetylcysteine (NAC) blocked BCB-induced ROS production and cell death. Therefore, these results indicate that BCB-induced apoptosis is mediated by a caspase dependent pathway and ROS production in HepG2 cells.

Keywords

References

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