Neuroprotective effects of sulforaphane in an in vitro model of Parkinson\u2019s disease

There is growing interest in dietary strategies aimed at counteracting oxidative stress induced neuronal death associated with Parkinson's disease (PD). Isothiocyanates (ITCs), present in Cruciferous vegetables, are known as cancer chemopreventive agents and strong inducers of phase II detoxification enzymes. Among the various ITCs, sulforaphane (SUL) has recently gained attention as a potential neuroprotective agent. In this study, we investigated the mechanism basis of the neuroprotective potential of SUL in a neuronal cell model of PD. In particular, we demonstrated that treatment of human neuronal like SH-SY5Y cells with SUL prevents the oxidative damage and neuronal death induced by 6-hydroxidopamine (6-OHDA), a specific neurotoxin. In parallel, we found a potent indirect antioxidant activity of SUL on neuronal cells that could be ascribed to increased GSH levels and phase II enzyme activities, such as glutathione-S-transferase, gutathione reductase and NADPH-quinone oxidoreductase. Interestingly, SUL also showed an ability to rescue the neuronal death induced by 6-OHDA through the activation of neuronal survival pathways such as PI3K/AKT and MEK/ERK. Taken together, these findings suggest thath SUL may have a positive impact on PD to retard or reverse the accellerated rate of neuronal degeneration

Sulforaphane counteracts oxidative stress induced apoptosis in human neuronal cells

Oxidative stress is a common feature of neurodegenerative diseases, such as Alzheimer's diseases (AD) and Parkinson's diseases (PD), causing the dysfunction or death of neuronal cells. Epidemiological evidence suggest that dietary antioxidants may act as disease-modifying neuroprotective compounds. Sulphoraphane (SUL), an isothiocyanate naturally found in Cruciferous vegetables, is a potent chemopreventive agent with a wide array of biological activities. In our experiments, SUL was found to protect human neuroblastoma SH-SY5Y cells from damage induced by 6-OHDA, a Parkinson specific neurotoxin. Pre-treatment of SH-SY5Y cells with SUL showed a significant concentration-dependent inhibition of apoptotic events, such as mitochondrial activity loss, translocation of phosphatidyl serine and DNA fragmentation increase . These neuroprotective effects were maintained for 24 h after the removal of SUL. Treated cells showed a significant increase of antioxidant activity of cytosolic fraction, glutathione levels and of other antioxidant enzymes (glutathione-S-transferase, glutathione reductase and NADPH-quinone reductase). Results also demonstrated that treatment of neurons with SUL after 6-OHDA treatment showed a significant decrease of apoptosis. SUL neuroprotective effects were mediated by activation (phosphorylation) of ERK 1/2 and Akt kinase. Results encourage further research in PD animal models to explore the potential profile of SUL as novel neuroprotective agent