alexa A phospholipase C-dependent intracellular Ca2+ release pathway mediates the capsaicin-induced apoptosis in HepG2 human hepatoma cells.
Materials Science

Materials Science

Journal of Nanomedicine & Nanotechnology

Author(s): Kim JA, Kang YS, Lee YS

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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.
This article was published in Arch Pharm Res and referenced in Journal of Nanomedicine & Nanotechnology

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