Ginsenoside-Rh2-induced mitochondrial depolarization and apoptosis are associated with reactive oxygen species-and Ca2+-mediated c-Jun NH2-terminal kinase 1 activation in HeLa cells
- Authors
- Ham, Young-Mi; Lim, Jin-Hee; Na, Hye-Kyung; Choi, Joon-Seok; Park, Byoung-Duck; Yim, Hyungshin; Lee, Seung-Ki
- Issue Date
- Dec-2006
- Publisher
- AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
- Citation
- JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, v.319, no.3, pp.1276 - 1285
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
- Volume
- 319
- Number
- 3
- Start Page
- 1276
- End Page
- 1285
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/44467
- DOI
- 10.1124/jpet.106.109926
- ISSN
- 0022-3565
- Abstract
- We show here that Ca2+ and reactive oxygen species (ROS) are involved in the up-regulation of c-Jun NH2-terminal kinase 1 (JNK1) activity during apoptosis induced by ginsenoside Rh2 (G-Rh2) in HeLa, MCF10A-ras, and MCF7 cells. Addition of antioxidants such as N-acetyl-L-cysteine or catalase attenuates G-Rh2-induced ROS generation, JNK1 activation, and apoptosis. The overexpression of catalase down-regulates caspase-3 and JNK1 activities. G-Rh2 treatment of cells results in mitochondrial depolarization, second mitochondrial activator of caspase release, and translocation of Bax into the mitochondria, and these events are inhibited by antioxidants. Ca2+ is also involved in mitochondrial depolarization during G-Rh2-induced apoptosis. These results suggest that ROS and Ca2+ are important signaling intermediates leading to stress- activated protein kinase/extracellular signal-regulated kinase kinase 1/JNK1 activation and depolarization of the mitochondrial membrane potential in G-Rh2-induced apoptosis.
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