Prevention of UV Radiation-Induced Premature Skin Aging in Hairless Mice by the Novel Compound Melanocin A

Authors

  • Chi-Hyun Park,

    1. Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea
    2. Laboratory of Cutaneous Aging Research, Clinical Research Institute, Seoul National University Hospital, Seoul, Korea
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  • Min Jung Lee,

    1. Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea
    2. Laboratory of Cutaneous Aging Research, Clinical Research Institute, Seoul National University Hospital, Seoul, Korea
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  • Jong-Pyung Kim,

    1. Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea
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  • Ick Dong Yoo,

    1. Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea
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  • Jin Ho Chung

    Corresponding author
    1. Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea
    2. Laboratory of Cutaneous Aging Research, Clinical Research Institute, Seoul National University Hospital, Seoul, Korea
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ABSTRACT

Repetitive exposure of the skin to UV radiation induces various harmful changes, such as thickening, wrinkle formation, inflammation and carcinogenesis. A variety of natural compounds and synthetic compounds have been studied to determine whether they can prevent W-induced harmful effects. In this study, we investigated the effect of a novel compound, Melanocin A, which was isolated from Eupenicillium shearii F80695, on UV-induced premature skin aging. First, we studied the effect of Melanocin A on UV-induced matrix metalloproteinase (MMP)-9 expression in an immortalized human keratinocyte cell line, HaCaT, in vitro. Acute UV irradiation induced MMP-9 expression at both the mRNA and protein levels and Melanocin A suppressed this expression in a dose-dependent manner. We then investigated the effect of Melanocin A on UV-induced skin changes in hairless mice in vivo. Chronic exposure of hairless mouse dorsal skin to UV increased skin thickness and induced wrinkle formation and the gelatinase activities of MMP-2 and MMP-9. Moreover, Melanocin A significantly suppressed UV-induced morphologic skin changes and MMP-2 and MMP-9 expression. Taken together, these results show that Melanocin A can prevent the harmful effects of UV that lead to skin aging. Therefore, we suggest that Melanocin A should be viewed as a potential therapeutic agent for preventing and/or treating premature skin aging.

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