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• W2121458082 abstract "We show here that Ca(2+) and reactive oxygen species (ROS) are involved in the up-regulation of c-Jun NH(2)-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. Ca(2+) is also involved in mitochondrial depolarization during G-Rh2-induced apoptosis. These results suggest that ROS and Ca(2+) 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." @default.
• W2121458082 created "2016-06-24" @default.
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• W2121458082 date "2006-09-14" @default.
• W2121458082 modified "2023-09-24" @default.
• W2121458082 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" @default.
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• W2121458082 doi "https://doi.org/10.1124/jpet.106.109926" @default.
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