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.
D. Vauzour, M. Buonfiglio, G. Corona, J. Chirafisi, K. Vafeiadou, C. Angeloni, et al. (2014). Sulforaphane Protects Cortical Neurons against Endogenous Neurotoxins in a Model of Parkinson’s Disease. Leuven : International Society for Horticultural Science.
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.
