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Apoptotic Effects and Mechanism Study of Scopoletin in HepG2 Cells  

Kwon Kang-Beom (Department of Physiology, School of Oriental Medicine, Wonkwang University)
Kim Eun-Kyung (Department of Physiology, School of Oriental Medicine, Wonkwang University)
Park Sung-Joo (Department of herbology, School of Oriental Medicine, Wonkwang University)
Song Ho-Joon (Department of herbology, School of Oriental Medicine, Wonkwang University)
Lee Young-Rae (Department of Biochemistry, Institute for Healthcare Technology Development, Medical School, Chonbuk National University)
Park Byung-Hyun (Department of Biochemistry, Institute for Healthcare Technology Development, Medical School, Chonbuk National University)
Park Jin-Woo (Department of Biochemistry, Institute for Healthcare Technology Development, Medical School, Chonbuk National University)
Ryu Do-Gon (Department of Physiology, School of Oriental Medicine, Wonkwang University)
Publication Information
Journal of Physiology & Pathology in Korean Medicine / v.19, no.6, 2005 , pp. 1594-1598 More about this Journal
Abstract
Scopoletin (6-methoxy-7-hydrorycournarin) is a phenolic coumarin and a member of the phytoalexins. In this study we investigated whether scopoletin causes apoptosis in human hepatoma HepG2 cells and, if so, by what mechanisms. We report that scopoletin induced apoptosis as confirmed by a chromatin condensation. The signal cascade acivated by scopoletin included the activation of caspase-3 as evidenced by increased pretense activity. Activation of caspase-3 resulted in the cleavage of 116 kDa poly(ADP-ribose) polymerase (PARP) to 85 kDa cleavage product in a dose-dependent fashion. Also, scopoletin-induced apoptotic mechanism of HepG2 cells involved the generation of hydrogen peroxide. Taken together, these results suggest that scopgletin induces hydrogen peroxide generation, which, in turn, causes activation of caspase-3, degradation of PARP, and eventually leads to apoptotic cell death in HepG2 cells.
Keywords
scopoletin; HepG2 cells; apoptosis; caspase-3; PARP; hydrogen peroxide;
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