Effects of sulforaphane in the central nervous system

Sulforaphane (SFN) is an active component extracted from vegetables like cauliflower and broccoli. Activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling is a common mechanism for the anti-oxidative and anti-inflammatory activity of some herb-derived compounds, such as icariin and berberine. However, due to its peculiar ability in Nrf2 activation, SFN is recognized as an activator of Nrf2 and recommended as a supplementation for prevention and/or treatment of disorders like neoplasm and heart failure. In the central nervous system (CNS), the prophylactic and/or therapeutic effects of SFN have been revealed in recent years. For example, it has been reported to prevent the progression of Alzheimer's disease, Parkinson's disease, cerebral ischemia, Huntington's disease, multiple sclerosis, epilepsy, and psychiatric disorders via promotion of neurogenesis or inhibition of oxidative stress and neuroinflammation. SFN is also implicated in reversing cognition, learning, and memory impairment in rodents induced by scopolamine, lipopolysaccharide, okadaic acid, and diabetes. In models of neurotoxicity, SFN has been shown to suppress neurotoxicity induced by a wide range of toxic factors, such as hydrogen peroxide, prion protein, hyperammonemia, and methamphetamine. To date, no consolidated source of knowledge about the pharmacological effects of SFN in the CNS has been presented in the literature. In this review, we summarize and discuss the pharmacological effects of SFN as well as their possible mechanisms in prevention and/or therapy of disorders afflicting the CNS, aiming to get a further insight into how SFN affects the pathophysiological process of CNS disorders.