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Parkinson's disease (PD) is a progressive neurodegenerative disorder withselective loss of dopaminergic neurons in the substantia nigra. Evidence suggeststhat oxidative stress is involved in the pathogenesis of PD. Sulforaphane (SF),a naturally occurring isothiocyanate, has been shown to protect against oxidativestress by inducing the expression of various NF-E2-related factor-2 (Nrf2) responsivegenes. Previous studies have shown that SF protects dopaminergic neurons againstPD-related neurotoxin 6-hydroxydopamine (6-OHDA)-induced cytotoxicity. However,the molecular mechanisms by which SF protects against 6-OHDA-induced cytotoxicityare poorly elucidated. In this study, we found that pretreatment with SF significantlyreduced 6-OHDA-induced caspase-3 activation and subsequent cell death. SF alsoincreased heme oxygenase-1 (HO-1) expression, which conferred protection against6-OHDA-induced cytotoxicity. Furthermore, SF induced the translocation of Nrf2into the nucleus and activated PI3K/Akt, a pathway that is involved in SF-inducedNrf2 nuclear translocation, HO-1 expression and cytoprotection. These resultssuggest that SF inhibits 6-OHDA-induced cytotoxicity through increasing HO-1 expressionin a PI3K/Akt-dependent manner.

Sulforaphane protects against 6-hydroxydopamine-induced cytotoxicity by increasing expression of heme oxygenase-1 in a PI3K/Akt-dependent manner