Abstract

UVB exposure is one of the causes of several skin complications including but not limited to premature aging, wrinkle formation, and hyperpigmentation. UV-induced skin aging is called photoaging, and oxidative stress-induced overexpression of matrix metalloproteinases (MMPs) is the main reason behind the photoaging-mediated collagen degradation. Natural origin inhibitors of MMPs are regarded as a promising approach to prevent or treat photoaging. Therefore, the present study investigated the protective effects of 3,5-dicaffeoyl-epi-quinic acid (DCEQA) in human HaCaT keratinocytes against UVB irradiation-related dysregulation of MMPs. Changes in the mRNA and protein expression and release of MMP-1, -2, and -9 were observed after UVB irradiation with or without DCEQA treatment. In addition, the effect of DCEQA on the activation of p38, JNK, and ERK MAPKs was analyzed. Treatment of UVB-irradiated HaCaT cells with 10 μM DCEQA significantly suppressed the overexpression of both mRNA and protein of MMP-1, -2, and -9 while slightly increasing the diminished type I procollagen production. UVB-induced activation of MAPKs was also ameliorated by DCEQA treatment in a dose-dependent manner. Results indicated that DCEQA treatment was able to protect keratinocytes from UVB-induced photoaging by inhibiting the stimulated production of MMPs and the related decrease in collagen production. It was suggested that DCEQA downregulated the collagen degradation via inhibition of MAPK activation, which resulted in decreased MMP activity.

Highlights

  • Jung Hwan Oh,1 Jung Im Lee,1 Fatih Karadeniz,1 So Young Park,2 Youngwan Seo,3 and Chang-Suk Kong 1,2

  • Natural origin inhibitors of matrix metalloproteinases (MMPs) are regarded as a promising approach to prevent or treat photoaging. erefore, the present study investigated the protective effects of 3,5-dicaffeoyl-epi-quinic acid (DCEQA) in human HaCaT keratinocytes against Ultraviolet B (UVB) irradiation-related dysregulation of MMPs

  • Results indicated that DCEQA treatment was able to protect keratinocytes from UVB-induced photoaging by inhibiting the stimulated production of MMPs and the related decrease in collagen production

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Summary

Introduction

Jung Hwan Oh, Jung Im Lee, Fatih Karadeniz, So Young Park, Youngwan Seo, and Chang-Suk Kong 1,2. Treatment of UVB-irradiated HaCaT cells with 10 μM DCEQA significantly suppressed the overexpression of both mRNA and protein of MMP-1, -2, and -9 while slightly increasing the diminished type I procollagen production. Results indicated that DCEQA treatment was able to protect keratinocytes from UVB-induced photoaging by inhibiting the stimulated production of MMPs and the related decrease in collagen production. UVB-irradiated keratinocytes were shown to overexpress MMPs via ROS-mediated MAPK activation. Overproduction of MMPs in keratinocytes exposed to harmful doses of UVB results in diminished collagen production and increased cleavage of ECM components such as collagen and elastin. E current study is aimed at evaluating the photoprotective effect of DCEQA against UVB-induced changes in skin cells and analyzing its possible mechanism of action for antiphotoaging potential As a part of our continuous effort to develop natural products with bioactivities, 3,5-dicaffeoyl-epi-quinic acid (DCEQA), a bioactive derivative of CQA, has been shown to possess antiobesity [21] and photoprotective antioxidant abilities [22]. e current study is aimed at evaluating the photoprotective effect of DCEQA against UVB-induced changes in skin cells and analyzing its possible mechanism of action for antiphotoaging potential

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