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Rosa gallica and its active compound, cyanidin‐3,5‐O‐diglucoside, improve skin hydration via the GLK signaling pathway

Rosa gallica has been previously reported to display anti‐inflammatory, anti‐oxidative, and anti‐skin wrinkle activities. However, the effect of Rosa gallica on skin hydration and its active components are largely unknown. Herein, we aimed to investigate the skin hydration effect of rose petal extra...

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Bibliographic Details
Published in:BioFactors (Oxford) 2023-03, Vol.49 (2), p.415-427
Main Authors: Seo, Ji‐Won, Jo, Seongin, Jung, Young Sung, Mijan, Mohammad‐Al, Cha, Joy, Hong, Seungpyo, Byun, Sanguine, Lim, Tae‐Gyu
Format: Article
Language:English
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Summary:Rosa gallica has been previously reported to display anti‐inflammatory, anti‐oxidative, and anti‐skin wrinkle activities. However, the effect of Rosa gallica on skin hydration and its active components are largely unknown. Herein, we aimed to investigate the skin hydration effect of rose petal extract (RPE) in humans and elucidate the underlying molecular mechanism. A double‐blinded clinical study was performed to investigate the effect of RPE on skin hydration. Stratum corneum moisture analysis demonstrated that RPE treatment significantly improved hydration levels in human skin. Furthermore, HAS2 and hyaluronic acid levels were notably increased by RPE in keratinocytes and 3D human skin equivalent model. By comparing the modulatory effect on HAS2 expression, cyanidin‐3,5‐O‐diglucoside (CDG) was identified as the most potent compound in RPE likely responsible for skin hydration. The kinase activity of GLK, an upstream regulator of MAPK signaling, was increased by CDG in a dose‐dependent manner. Importantly, silencing GLK reversed CDG‐mediated HAS2 upregulation, further supporting the involvement of GLK in the CDG‐mediated effects. Binding of CDG to GLK was confirmed by pull‐down assay and computer modeling. These findings suggest that RPE and its active component CDG increases skin hydration by upregulating HAS2 expression through modulating the GLK‐MAP2K‐MAPK signaling pathway.
ISSN:0951-6433
1872-8081
DOI:10.1002/biof.1922