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

• Published in: International journal of molecular sciences 2020-10, Vol.21 (20), p.7756
• Main Authors: Oh, Jung Hwan, Karadeniz, Fatih, Kong, Chang-Suk, Seo, Youngwan
• Format: Article
• Language: English
• Subjects: Acids; Aging; Aging (artificial); Aging (natural); Biodegradation; Cell Line; Chlorogenic Acid - analogs & derivatives; Chlorogenic Acid - pharmacology; Collagen; Collagen (type I); Collagen - genetics; Collagen - metabolism; Collagen Type I - genetics; Collagen Type I - metabolism; Cytotoxicity; Dermis - cytology; Enzymes; Fibroblasts - drug effects; Fibroblasts - metabolism; Fibroblasts - radiation effects; Gelatinase B; Gene Expression - drug effects; Gene Expression - radiation effects; Humans; Interstitial collagenase; Kinases; MAP kinase; MAP Kinase Signaling System - drug effects; MAP Kinase Signaling System - genetics; MAP Kinase Signaling System - radiation effects; Matrix metalloproteinase; Matrix Metalloproteinase 1 - genetics; Matrix Metalloproteinase 1 - metabolism; Matrix Metalloproteinase 3 - genetics; Matrix Metalloproteinase 3 - metabolism; Matrix Metalloproteinase 9 - genetics; Matrix Metalloproteinase 9 - metabolism; Matrix metalloproteinases; Molecular modelling; Nuclear transport; Phosphorylation; Photodegradation; Physiology; Procollagen; Proteins; Quinic acid; Radiation damage; Skin; Skin Aging - drug effects; Skin Aging - radiation effects; Smad protein; Stromelysin 1; Transcription Factor AP-1 - genetics; Transcription Factor AP-1 - metabolism; Transcription factors; Ultraviolet radiation; Ultraviolet Rays
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21207756

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.