KMID : 0613820150250040416
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Journal of Life Science 2015 Volume.25 No. 4 p.416 ~ p.424
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Apoptotic Effect of Pinosylvin at a High Concentration Regulated by c-Jun N-Terminal Kinase in Bovine Aortic Endothelial Cells
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Song Ji-Na
Park Jin-Sun Jeong Eun-Sil So A-Young Pyee Jae-Ho Park Heon-Yong
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Abstract
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Pinosylvin is a stilbenoid found in the Pinus species. Pinosylvin at ~pM to ~nM concentrations induces cell proliferation, cell migration and anti-inflammatory activity in endothelial cells. However, it was recently reported that pinosylvin at high concentrations (50 to 100 ¥ìM) induces cell death in bovine aortic endothelial cells. In this study, we conducted a series of experiments to discover how pinosylvin at a high concentration (50 ¥ìM) induces endothelial cell death. Pinosylvin at the high concentration was shown to induce endothelial cell apoptosis through enhancing caspase-3 activity, flip-flop of phosphatidyl serine, and nuclear fragmentation. We found that pinosylvin at the high concentration additively increased caspase-3 activity enhanced by serum-starvation or treatment with 100 ¥ìM etoposide. We also determined that pinosylvin at the high concentration promoted activations of c-Jun N-terminal kinase (JNK) and endothelial nitric oxide synthetase (eNOS). We further ran a series of experiments to find out which signaling molecule plays a critical role in the pinosylvin-induced apoptosis. We finally found that SP-600125, a JNK inhibitor, had an inhibitory effect on the pinosylvin-induced endothelial cell death, but L-NAME, an eNOS inhibitor, had no effect. These data indicate that JNK is involved in the pinosylvin-induced apoptosis. Collectively, pinosylvin at high doses induces cell apoptosis via JNK activation.
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KEYWORD
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Apoptosis, cell death, c-Jun N-terminal kinase, endothelial cells, pinosylvin
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