Archives of Pharmacal Research

  • 제28권7호
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  • Pages.784-790
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  • 2005
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  • 0253-6269(pISSN)
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  • 1976-3786(eISSN)
대한약학회 (The Pharmaceutical Society of Korea)
권호 표지

Protective Effects of EGCG on UVB-Induced Damage in Living Skin Equivalents

  • Kim, So-Young (Department of Dermatology, Seoul National University College of Medicine) ;
  • Kim, Dong-Seok (Department of Dermatology, Seoul National University College of Medicine, Research Division for Human Life Sciences, Seoul National University) ;
  • Kwon, Sun-Bang (Welskin Co. Ltd.) ;
  • Park, Eun-Sang (Department of Dermatology, Seoul National University College of Medicine) ;
  • Huh, Chang-Hun (Department of Dermatology, Seoul National University College of Medicine) ;
  • Youn, Sang-Woong (Department of Dermatology, Seoul National University College of Medicine) ;
  • Kim, Suk-Wha (Department of Plastic and Reconstructive Surgery, Seoul National University College of Medicine) ;
  • Park, Kyoung-Chan (Department of Dermatology, Seoul National University College of Medicine)
  • 발행 : 2005.07.01
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초록

In this study, we evaluate the effects of (-)-epigallocatechin-3-gallate (EGCG) on ultraviolet B(UVB)-irradiated living skin equivalents (LSEs). Histologically, UVB irradiation induced thinning of the LSE epidermis, whereas EGCG treatment led to thickening of the epidermis. Moreover, EGCG treatment protected LSEs against damage and breakdown caused by UVB exposure. Immunohistochemically, UVB-exposed LSEs expressed p53, Fas, and 8-hydroxy-deoxyguanosine (8-OHdG), all of which are associated with apoptosis. However, EGCG treatment reduced the levels of UVB-induced apoptotic markers in the LSEs. In order to determine the signaling pathways induced by UVB, Western blot analysis was performed for both c-Jun $NH_2$-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), which are associated with UVB-induced oxidative stress. UVB activated JNK in the epidermis and dermis of the LSEs, and EGCG treatment reduced the UVB-induced phosphorylation of JNK. In addition, p38 MAPK was also found to have increased in the UVB-exposed LSEs. Also, EGCG reduced levels of the phosphorylation of UVB-induced p38 MAPK. In conclusion, pretreatment with EGCG protects against UVB irradiation via the suppression of JNK and p38 MAPK activation. Our results suggest that EGCG may be useful in the prevention of UVB-induced human skin damage, and LSEs may constitute a potential substitute for animal and human studies.

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