Oral Administration of Rosa gallica Prevents UVB-Induced Skin Aging through Targeting the c-Raf Signaling Axis.

Seongin Jo,Sanguine Byun,Ye-Ryeong Cho,Won-Chul Lim,Ji-Won Seo,Tae-Gyu Lim,Young-Sung Jung,Tae-Gyu Nam

doi:10.3390/antiox10111663

Abstract

Rosa gallica is a widely used Rosa species for medicinal and culinary purposes. Rosa gallica has been reported to display antioxidant, anti−inflammatory, and antibacterial activities. However, the effect of Rosa gallica against skin aging in vivo is unknown and its active components have not been fully understood. Oral administration of Rosa gallica prevented UVB−mediated skin wrinkle formation and loss of collagen/keratin fibers in the dorsal skin of mice. Examination of biomarkers at the molecular level showed that Rosa gallica downregulates UVB−induced COX−2 and MMP−1 expression in the skin. Through a direct comparison of major compounds identified using the UHPLC−MS/MS system, we discovered gallic acid as the primary component contributing to the anti-skin aging effect exhibited by Rosa gallica. Examination of the molecular mechanism revealed that gallic acid can potently and selectively target the c−Raf/MEK/ERK/c−Fos signaling axis. In addition, both gallic acid and MEK inhibitor blocked UVB−induced MMP−1 expression and restored collagen levels in a reconstructed 3D human skin model. Collectively, Rosa gallica could be used as a functional ingredient in the development of nutraceuticals against skin aging.

Highlights

Chronic irradiation of ultraviolet B (UVB) light causes skin wrinkle formation, inflammation, pigmentation, and dehydration [1,2]
These results clearly show that oral intake of Rosa gallica Petal Extract (RPE) can suppress UVB−mediated skin aging in vivo
While there has been a previous report that RPE can attenuate matrix metalloproteinases (MMPs)−1 in cells, this is the first time to show that RPE can suppress MMP−1 expression as well as collagen degradation and wrinkle formation in vivo

Summary

Introduction

Chronic irradiation of ultraviolet B (UVB) light causes skin wrinkle formation, inflammation, pigmentation, and dehydration [1,2]. UVB triggers signaling pathways leading to upregulation of genes involved in collagen degradation and inflammation [1,3]. Matrix metalloproteinases (MMPs), especially MMP−1, play a key role in promoting collagen degradation and in turn, wrinkle formation [4]. Cyclooxygenase 2 (COX−2), which can be induced by UVB light, mediates skin inflammation and photoaging [5]. Food compounds that can inhibit the expression of MMP−1 or/and COX−2 have the potential to possess anti-skin aging effects [6,7]. Activator protein 1 (AP−1) and its upstream regulatory pathways have been known to be major contributing factors to MMP–1 expression and skin aging [8]. AP−1 is a dimeric transcription factor formed by Fos (c−Fos, FosB, Fra, and Fra2) and Jun

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Conclusion