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Antiphotoaging Effect of 3,5-Dicaffeoyl-epi-quinic Acid against UVA-Induced Skin Damage by Protecting Human Dermal Fibroblasts In Vitro

1
Marine Biotechnology Center for Pharmaceuticals and Foods, College of Medical and Life Sciences, Silla University, Busan 46958, Korea
2
Department of Food and Nutrition, College of Medical and Life Sciences, Silla University, Busan 46958, Korea
3
Division of Marine Bioscience, College of Ocean Science and Technology, Korea Maritime and Ocean University, Busan 49112, Korea
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(20), 7756; https://doi.org/10.3390/ijms21207756
Received: 21 August 2020 / Revised: 15 October 2020 / Accepted: 16 October 2020 / Published: 20 October 2020
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
Cutaneous aging is divided into intrinsic and exogenous aging correspondingly contributing to the complex biological phenomenon in skin. Intrinsic aging is also termed chronological aging, which is the accumulation of inevitable changes over time and is largely genetically determined. Superimposed on this intrinsic process, exogenous aging is associated with environmental exposure, mainly to ultraviolet (UV) radiation and more commonly termed as photoaging. UV-induced skin aging induces increased expression of matrix metalloproteinases (MMPs) which in turn causes the collagen degradation. Therefore, MMP inhibitors of natural origin are regarded as a primary approach to prevent or treat photoaging. This study investigated the effects of 3,5-dicaffeoyl-epi-quinic acid (DEQA) on photoaging and elucidated its molecular mechanisms in UVA-irradiated human dermal fibroblasts (HDFs). The results show that treatment with DEQA decreases MMP-1 production and increases type I collagen production in UVA-damaged HDFs. In addition, treatment of UVA-irradiated HDFs with DEQA downregulates MMP-1, MMP-3 and MMP-9 expression via blocking MAPK-cascade-regulated AP-1 transcriptional activity in UVA-irradiated HDFs. Furthermore, DEQA relieves the UVA-mediated suppression of type I procollagen and collagen expression through stimulating TGF-β/Smad signaling, leading to activation of the Smad 2/3 and Smad 4 nuclear translocation. These results suggest that DEQA could be a potential cosmetic agent for prevention and treatment of skin photoaging. View Full-Text
Keywords: 3,5-Dicaffeoyl-epi-quinic acid; human dermal fibroblasts; matrix metalloproteinases; photoaging; UVA 3,5-Dicaffeoyl-epi-quinic acid; human dermal fibroblasts; matrix metalloproteinases; photoaging; UVA
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MDPI and ACS Style

Oh, J.H.; Karadeniz, F.; Kong, C.-S.; Seo, Y. Antiphotoaging Effect of 3,5-Dicaffeoyl-epi-quinic Acid against UVA-Induced Skin Damage by Protecting Human Dermal Fibroblasts In Vitro. Int. J. Mol. Sci. 2020, 21, 7756. https://doi.org/10.3390/ijms21207756

AMA Style

Oh JH, Karadeniz F, Kong C-S, Seo Y. Antiphotoaging Effect of 3,5-Dicaffeoyl-epi-quinic Acid against UVA-Induced Skin Damage by Protecting Human Dermal Fibroblasts In Vitro. International Journal of Molecular Sciences. 2020; 21(20):7756. https://doi.org/10.3390/ijms21207756

Chicago/Turabian Style

Oh, Jung H., Fatih Karadeniz, Chang-Suk Kong, and Youngwan Seo. 2020. "Antiphotoaging Effect of 3,5-Dicaffeoyl-epi-quinic Acid against UVA-Induced Skin Damage by Protecting Human Dermal Fibroblasts In Vitro" International Journal of Molecular Sciences 21, no. 20: 7756. https://doi.org/10.3390/ijms21207756

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