Tier 4 — mechanistic

Fisetin inhibits UVB-induced cutaneous inflammation and activation of PI3K/AKT/NFκB signaling pathways in SKH-1 hairless mice

Pal HC, Athar M, Elmets CA, Afaq F

Photochemistry and Photobiology 2015 91(1):225-234

Bibliography

PubMed: PMID 25169110
PubMed Central: PMC4294956
DOI: 10.1111/php.12337
Funding: Not stated in the available abstract.
Competing interests: Not stated in the available abstract.

Study snapshot

Design	In vivo animal study
Model	SKH-1 hairless mice, UVB irradiation
Sample	Not applicable (animal study)
Intervention	Topical fisetin application before/after UVB exposure
Duration	Acute/short-term UVB exposure protocol
Endpoints	Cutaneous inflammation; PI3K/AKT/NF-kB pathway activation; Skin oedema and inflammatory markers

What the study showed, in plain terms

This mouse study found that applying fisetin to skin before UV exposure reduced sunburn-type inflammation. It worked partly by blocking a signalling pathway (PI3K/AKT/NF-kB) that drives inflammation after UV damage, adding mechanistic detail to why topical fisetin might protect skin from sun damage.

Key findings

Topical fisetin application inhibited UVB-induced cutaneous inflammation in SKH-1 hairless mice, in part through inhibition of the PI3K/AKT/NF-kB signalling pathway. This adds mechanistic detail complementary to the Nrf2-pathway findings reported by Wu et al. 2017 in a related hairless-mouse UVB model.

What this study can and cannot tell us

Mouse model only, no human data. Topical-only intervention; does not address oral fisetin bioavailability to skin.

Citation network

Articles citing this research paper

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Biohack Blueprint analyses that reference this study in their evidence base.

Jul 11, 2026 Fisetin for Skin: Antioxidant, Senolytic, and TopicalFisetin has preclinical skin evidence from UVB, dermal-senescence and diabetic-wound models. A 2026 topical mouse study improved dermal/granulation balance and reduced fibrosis...Read analysis

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