Induction of apoptosis by 2,3-dehydrosilybin via a caspase-dependent pathway in human HeLa cells
- Authors
- Cho, Byoung Ok; So, Yangkang; Jin, Chang Hyun; Byun, Myung Woo; Seo, Kwon Il; Ko, Kisung; Chun, Myoung Sook; Jeong, Il Yun
- Issue Date
- Feb-2014
- Publisher
- TAYLOR & FRANCIS LTD
- Keywords
- 2,3-dehydrosilybin; apoptosis; caspase; cytochrome c; mitochondrial membrane potential(Delta psi(m))
- Citation
- BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY, v.78, no.2, pp 255 - 262
- Pages
- 8
- Journal Title
- BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
- Volume
- 78
- Number
- 2
- Start Page
- 255
- End Page
- 262
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/12568
- DOI
- 10.1080/09168451.2014.885828
- ISSN
- 0916-8451
1347-6947
- Abstract
- The aim of this study was to investigate the mechanisms involved in the apoptosis of HeLa cells due to 2,3-dehydrosilybin (DHS) treatment. DHS treatment over 24 h significantly inhibited cell viability and induced apoptosis in a dose-dependent manner. It also triggered the cleavage of caspase-8, caspase-9, caspase-3, and PARP, and significantly increased caspase-3 activity in a dose-dependent manner. Moreover, it triggered the depolarization of the mitochondrial membrane potential (Delta psi(m)), the release of cytochrome c into the cytosol, the cleavage of Bid, and the downregulation of Bcl-2 in a dose-dependent manner. Furthermore, z-VAD-fmk (a pan-caspase inhibitor) and z-IETD-fmk (a specific caspase-8 inhibitor) abolished the DHS-induced activation of the caspase-8, -9, and -3, cleavage of PARP, the depolarization of Delta psi(m), the release of cytochrome c, the cleavage of Bid, and the downregulation of Bcl-2. Taken together, these results suggest that DHS-induced apoptosis is mediated by a caspase-dependent pathway in human HeLa cells.
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