Ageing is a natural process that we all experience, but the quest for ways to slow down or even reverse its effects has been a perennial pursuit of humanity. One promising area of research in the realm of ageing is the study of sulforaphane, a natural compound found in cruciferous vegetables like broccoli, brussels sprouts, and kale.
Over the years, a growing body of scientific research has explored the potential anti-ageing properties of sulforaphane, and the results have been nothing short of fascinating. In this blog post, we will delve into the findings of recent studies to shed light on the connection between sulforaphane and ageing.
Sulforaphane - role in ageing and neurodegeneration
GeroScience. 2019 Oct; 41(5): 655–670.
SFN activates the antioxidant and anti-inflammatory responses by inducing Nrf2 pathway and inhibiting NF-κB. It also has an epigenetic effect by inhibiting HDAC and DNA methyltransferases and modifies mitochondrial dynamics. Moreover, SFN preserves proteome homeostasis (proteostasis) by activating the proteasome, which has been shown to lead to increased cellular lifespan and prevent neurodegeneration.
SFN activates protective cellular responses, reducing inflammation and oxidative stress while promoting cellular health and longevity, particularly in the brain.
Sulforaphane reactivates cellular antioxidant defence by inducing Nrf2/ARE/Prdx6 activity during ageing and oxidative stress
Sci Rep. 2017; 7: 14130.
This study has shown that, in ageing, increased oxidative stress in lenses and lens cells is associated with failure of protective response due to dysregulation of Nrf2 and its target antioxidant gene Prdx6, and that this process was attenuated by application of Sulforaphane.
Sulforaphane and phenylethyl isothiocyanate protect human skin against UVR-induced oxidative stress and apoptosis: role of Nrf2-dependent gene expression and antioxidant enzymes
Pharmacol Res. 2013 Dec;78:28-40.
In this study, sulforaphane (SFN) and phenylethyl isothiocyanate (PEITC) were tested for their ability to counteract UVR-induced oxidative stress and apoptosis in ex vivo human full-thickness skin combined with in vitro HaCaT keratinocytes.
Mechanistic cell culture studies revealed SFN and PEITC to increase Nrf2 activity and Nrf2-dependent gene expression (γGCS, HO-1, NQO1); this was paralleled in human full skin mRNA. The induction of Nrf2-dependent antioxidant pathways seems to be a potential mechanism by which SFN and PEITC protect against UVR-induced oxidative stress and apoptosis in human skin.
