Capsaicin up-regulates pro-apoptotic activity of thiazolidinediones in glioblastoma cell line - 18/11/20
, Jerzy PalkaBienvenido a EM-consulte, la referencia de los profesionales de la salud.
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Graphical abstract |
Highlights |
• | Capsaicin induces apoptosis in glioblastoma LN-18 cells. |
• | Capsaicin-induced apoptosis is not dependent on TRPV1. |
• | Capsaicin increases PPARγ expression in glioblastoma LN-18 cells. |
• | Capsaicin and rosiglitazone/pioglitazone evoke synergistic pro-apoptotic effect. |
Abstract |
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.
El texto completo de este artículo está disponible en PDF.Keywords : Capsaicin, Apoptosis, Glioblastoma, Pioglitazone, Rosiglitazone, Troglitazone
Esquema
Vol 132
Artículo 110741- décembre 2020 Regresar al número
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Bienvenido a EM-consulte, la referencia de los profesionales de la salud.
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Bienvenido a EM-consulte, la referencia de los profesionales de la salud.
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