Capsaicin (N-vanillyl-8-methyl-alpha-nonenamide), a spicy, neurotoxic component of hot pepper is a ligand of vanilloid type-I (TRPV1) receptor of anti-cancer potential. However, molecular mechanism of its action is not fully understood. We found that capsaicin stimulated intrinsic and extrinsic pathway of apoptosis in human glioblastoma LN-18 cell line and this phenomenon was not dependent on TRPV1. Activation of peroxisome proliferator-activated receptor gamma (PPARγ), a ligand-dependent transcription factor, also induced apoptosis in glioblastoma cells. Although PPARγ ligands (thiazolidinediones - rosiglitazone, pioglitazone) promoted apoptosis in LN-18 cells, capsaicin augmented this effect. We found that capsaicin in a dose dependent manner induced expression of PPARγ in glioblastoma LN-18 cells. These findings suggest that capsaicin-dependent up-regulation of PPARγ represent the mechanism for augmentation of cell death by thiazolidinediones.
Keywords: Apoptosis; Capsaicin; Glioblastoma; Pioglitazone; Rosiglitazone; Troglitazone.
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