Abstract
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.
Highlights
As the population ages, general skin deterioration of the elderly demands more attention
The cytotoxic effect of dicaffeoyl-epi-quinic acid (DEQA) on human dermal fibroblasts (HDFs) was evaluated by MTT test
Fl2u.o5r. eEsffceecntcoef DmEicQroAscoonpCicololabgseenrvParotidounctvioenriifnieUdVtAha-ItrrcaodlilaatgedenHlDevFesls in UVA-irradiated cells treated with DEAQ were significantly increased compared to the control group. These results indicated that DEQAIhnaodradneratttoeneuvaatliunagteefftehcet opnrodteeccrtievaeseedffceocltlsagoefnDsyEnQtAhesaigsaininpsthopthoodtaomdeaggreaddHatDioFns.of collagen, an immunohistochemistry staining was performed on UVA-irradiated HDF
Summary
General skin deterioration of the elderly demands more attention. The various clinical, physiological and histologic changes that are common indicators of old skin are progressively involved in its vulnerability to environmental injury and disease This deterioration requires dermatological researchers to study the biological process underlying skin aging, and the process of photoaging that is, itself, a critical clinical problem. TGF-β induces generation of ECM proteins collagen and elastin [15], and it blocks the production of proteolytic enzymes involved in the degradation of collagens, such as MMP-1 and MMP-3 [14,16]. The present study was performed to investigate the antiphotoaging effect of DEQA on both MMPs and type I procollagen pathways in UVA-irradiated HDFs and to determine its underlying mechanism
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