Dietary supplementation with sulforaphane ameliorates skin aging through activation of the Keap1-Nrf2 pathway.
Level 5 - mechanism / opinion, no new human data
Preclinical animal study
PubMed 34271100 · doi:10.1016/j.jnutbio.2021.108817
What was done
Male C57BL6 young (2 months) and old (21 months) mice were treated for 3 months with a sulforaphane (SFN)-supplemented diet (442.5 mg/kg) or a control diet. Researchers assessed skin antioxidant capacities (Nrf2, NQO1, HO1 mRNA and protein expression), reactive oxygen species (ROS), matrix metalloproteinase-9 (MMP9) protein levels, skin layer thickness, and collagen deposition.
What was found
In old SFN-treated mice compared to controls: - Skin mRNA levels increased for Nrf2 (P < .001), NQO1 (P < .001), and HO1 (P < .01). - Skin Nrf2 protein expression increased (P < .01), whereas NQO1 and HO1 protein expression did not significantly change. - Skin ROS and MMP9 protein levels significantly decreased (P < .05). - Epidermal thickness showed no significant difference between old and young treated animals, while dermal thickness remained lower in old vs. young treated mice (P < .05). - Collagen deposition was significantly improved in young mice (P < .05) and structurally improved in old mice (P < .001).
Why it matters
This study provides preclinical evidence that oral sulforaphane activates the Keap1-Nrf2 pathway to decrease oxidative stress markers and preserve collagen integrity in aged rodent skin.
Limits
The study was conducted entirely in male mice, limiting direct translation to human aging, physiology, or dietary intake levels. Total sample size (n) is not reported in the abstract. Functional skin outcomes and longer-term safety were not evaluated.
Cited by
- supports Sulforaphane treatment upregulates RNA expression levels of Nrf2 and Keap1.