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Phloroglucinol Reduces Photodamage in Hairless Mice via Matrix Metalloproteinase Activity Through MAPK Pathway

Authors
Im, A-RangNam, Kung-WooHyun, Jin WonChae, Sungwook
Issue Date
Jan-2016
Publisher
American Society for Photobiology
Keywords
Phloroglucinol; Photodamage
Citation
Photochemistry and Photobiology, v.92, no.1, pp 173 - 179
Pages
7
Journal Title
Photochemistry and Photobiology
Volume
92
Number
1
Start Page
173
End Page
179
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/9482
DOI
10.1111/php.12549
ISSN
0031-8655
1751-1097
Abstract
We investigated the photoprotective activity of phloroglucinol on ultraviolet B (UVB)-induced deleterious effects in hairless mice in vivo. To assess the photoprotective effect of phloroglucinol, phloroglucinol-treated HR-1 hairless male mice were exposed to UVB irradiation. The inhibitory activity of phloroglucinol on wrinkle formation was determined by analysis of skin replicas, epidermal thickness based on histological examination and collagen damage. Matrix metalloproteinase-1 (MMP-1), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase (TIMP) mRNA levels were measured by real-time PCR. UVB induced transcription of proinflammatory cytokines, including interleukin-1 beta (IL-1, IL-6) and IL-8 (IL-8). The protective effects of phloroglucinol on UVB-induced skin photoaging were examined by measuring protein levels of MMPs and mitogen-activated protein (MAP) kinases. The results of these experiments suggest that phloroglucinol has a significant beneficial effect on the barrier function of the skin. In hairless mice, signs of photoaging and photodamage, including coarse wrinkle formation, epidermal thickness and elastic fiber degeneration, were reduced in severity by phloroglucinol application. The phloroglucinol-treated group showed remarkably decreased mRNA levels of MMP-1, MMP-9 and inflammatory cytokines in comparison with those of the UVB-induced group. Oral administration of phloroglucinol attenuated phosphorylation of MAP kinases, including extracellular signal-regulated kinase, c-Jun N-terminal kinase and p38.
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