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Protective effects of galangin against H2O2/UVB-induced dermal fibroblast collagen degradation via hsa-microRNA-4535-mediated TGFβ/Smad signaling
Galangin may protect skin cells from collagen breakdown caused by oxidative stress and UVB by involving microRNA-4535 and the TGF-beta/Smad signaling pathway
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Abstract
Galangin treatment significantly alleviated UVB-induced skin photodamage in mice at doses of 12 mg/kg and 24 mg/kg.
- Galangin improved cell viability and reduced signs of dermal aging in human dermal fibroblasts exposed to HO/UVB.
- Activation of the Smad2/3/4 complex was observed following galangin treatment in UVB-exposed cells.
- hsa-miR-4535 was identified as a candidate microRNA that targets Smad4 and is associated with TGFβ/Smad signaling.
- Topical application of galangin reduced epidermal hyperplasia, wrinkle formation, and skin senescence in mice.
- Findings suggest a potential role of hsa-miR-4535 in the photo-protective effects of galangin against UVB-induced damage.
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