Cardiomyocyte loss through apoptosis has been reported in a variety of cardiovascular diseases. Being a highly regulated cell death program its inhibition is cardioprotective. We previously demonstrated that sulforaphane (SF), present in many Cruciferous vegetables, boosts cell defence system acting as an indirect antioxidant. The aim of this study was to evaluate SF ability to modulate pro and anti-apoptotic proteins resulting in the inhibition of H2O2-induced apoptosis. SF treatment was able to protect cells against oxidative damage increasing cell viability, and decreasing apoptosis markers like DNA fragmentation and PS exposure. Accordingly, SF reduced bax translocation to mitochondria, cytochrome C release and caspase 3 activation in comparison to untreated cells. Specific protein kinases inhibitors revealed that SF protection is mainly mediated by Akt activation. Taken together these results show that a reduction in apoptotic cell death contributes to cardioprotection, suggesting SF as a promising nutraceutical in the prevention of oxidative stress related cardiac diseases.
E. Leoncini, C. Angeloni, M. Malaguti, E. Motori, S. Hrelia. (2009). Sulforaphane as an antiapoptotic nutraceutical in cardiac cells. CATANIA : s.n.
Sulforaphane as an antiapoptotic nutraceutical in cardiac cells
LEONCINI, EMANUELA;ANGELONI, CRISTINA;MALAGUTI, MARCO;MOTORI, ELISA;HRELIA, SILVANA
2009
Abstract
Cardiomyocyte loss through apoptosis has been reported in a variety of cardiovascular diseases. Being a highly regulated cell death program its inhibition is cardioprotective. We previously demonstrated that sulforaphane (SF), present in many Cruciferous vegetables, boosts cell defence system acting as an indirect antioxidant. The aim of this study was to evaluate SF ability to modulate pro and anti-apoptotic proteins resulting in the inhibition of H2O2-induced apoptosis. SF treatment was able to protect cells against oxidative damage increasing cell viability, and decreasing apoptosis markers like DNA fragmentation and PS exposure. Accordingly, SF reduced bax translocation to mitochondria, cytochrome C release and caspase 3 activation in comparison to untreated cells. Specific protein kinases inhibitors revealed that SF protection is mainly mediated by Akt activation. Taken together these results show that a reduction in apoptotic cell death contributes to cardioprotection, suggesting SF as a promising nutraceutical in the prevention of oxidative stress related cardiac diseases.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.