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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

Title
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
Author
임형신
Issue Date
2006-12
Publisher
AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
Citation
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, v. 319, No. 3, Page. 1276-1285
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.
URI
http://jpet.aspetjournals.org/content/319/3/1276.fullhttps://repository.hanyang.ac.kr/handle/20.500.11754/110034
ISSN
0022-3565; 1521-0103
DOI
10.1124/jpet.106.109926
Appears in Collections:
COLLEGE OF PHARMACY[E](약학대학) > PHARMACY(약학과) > Articles
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