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A phospholipase c-dependent intracellular ca2+ release pathway mediates the capsaicin-induced apoptosis in HepG2 human hepatoma cells

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Abstract

The effect of capsaicin on apoptotic cell death was investigated in HepG2 human hepatoma cells. Capsaicin induced apoptosis in time- and dose-dependent manners. Capsaicin induced a rapid and sustained increase in intracellular Ca2+ concentration, and BAPTA, an intracellular Ca2+ chelator, significantly inhibited capsaicin-induced apoptosis. The capsaicin-induced increase in the intracellular Ca2+ and apoptosis were not significantly affected by the extracellular Ca2+ chelation with EGTA, whereas blockers of intracellular Ca2+ release (dantrolene) and phospholipase C inhibitors, U-73122 and manoalide, profoundly reduced the capsaicin effects. Interestingly, treatment with the vanilloid receptor antagonist, capsazepine, did not inhibit either the increased capsaicin-induced Ca2+ or apoptosis. Collectively, these results suggest that the capsaicin-induced apoptosis in the HepG2 cells may result from the activation of a PLC-dependent intracellular Ca2+ release pathway, and it is further suggested that capsaicin may be valuable for the therapeutic intervention of human hepatomas.

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Correspondence to Yong Soo Lee.

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Kim, JA., Kang, Y.S. & Lee, Y.S. A phospholipase c-dependent intracellular ca2+ release pathway mediates the capsaicin-induced apoptosis in HepG2 human hepatoma cells. Arch Pharm Res 28, 73–80 (2005). https://doi.org/10.1007/BF02975139

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  • DOI: https://doi.org/10.1007/BF02975139

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