The endogenous neurotoxin 5-S-cysteinyl-dopamine (CysDA) has been linked to the degeneration of dopaminergic neurons in the Substantia nigra. Sulforaphane (SFN) is an isothiocyanate derived from cruciferous vegetables that has been proposed as a potential chemopreventive agent, although its effects on other cells are less clear. This study was undertaken to investigate the protective effects of SFN against CysDA-induced injury in primary cortical neurons. The results indicate that SFN protects primary cortical neurons against CysDA-induced injury by a mechanism involving the increased nuclear translocation of Nrf2 and the increased activity of phase II enzymes such as glutathione-S-transferase, glutathione reductase, and thioredoxine reductase. Moreover, the protection exerted by SFN appears to be mediated by the activation of the extracellular signal-regulated kinase 1 and 2 (ERK1/2) and Akt/protein kinase B (PKB) pathways.
Sulforaphane Protects Cortical Neurons against Endogenous Neurotoxins in a Model of Parkinson’s Disease / D. Vauzour; M. Buonfiglio; G. Corona; J. Chirafisi; K. Vafeiadou; C. Angeloni; S. Hrelia; P. Hrelia; J.P.E. Spencer. - In: ACTA HORTICULTURAE. - ISSN 0567-7572. - STAMPA. - 1040:(2014), pp. 341-348. (Intervento presentato al convegno III International Symposium on Human Health Effects of Fruits and Vegetables-FAVHEALTH 2009 tenutosi a Avignon (France) nel 18-21 Ottobre 2009).
Sulforaphane Protects Cortical Neurons against Endogenous Neurotoxins in a Model of Parkinson’s Disease
ANGELONI, CRISTINA;HRELIA, SILVANA;HRELIA, PATRIZIA;
2014
Abstract
The endogenous neurotoxin 5-S-cysteinyl-dopamine (CysDA) has been linked to the degeneration of dopaminergic neurons in the Substantia nigra. Sulforaphane (SFN) is an isothiocyanate derived from cruciferous vegetables that has been proposed as a potential chemopreventive agent, although its effects on other cells are less clear. This study was undertaken to investigate the protective effects of SFN against CysDA-induced injury in primary cortical neurons. The results indicate that SFN protects primary cortical neurons against CysDA-induced injury by a mechanism involving the increased nuclear translocation of Nrf2 and the increased activity of phase II enzymes such as glutathione-S-transferase, glutathione reductase, and thioredoxine reductase. Moreover, the protection exerted by SFN appears to be mediated by the activation of the extracellular signal-regulated kinase 1 and 2 (ERK1/2) and Akt/protein kinase B (PKB) pathways.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
