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KMID : 0616120170480040273
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Korean Journal of Pharmacognosy
2017 Volume.48 No. 4 p.273 ~ p.279
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Broussochalcone B from Broussonetia papyrifera Induce Apoptosis via Activation of a Caspase Cascade and Reactive Oxygen Species Production in Human HepG2 cells
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Park Jin-Ryang
Ryu Hyung-Won
Cho Byoung-Ok
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Abstract
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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.
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KEYWORD
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Broussochalcone B, Broussonetia papyrifera, Apoptosis, Caspase, Reactive oxygen species
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