SHERP

UVB-induced interleukin-18 production is downregulated by tannic acids in human HaCaT keratinocytes

Cited 0 time in webofscience Cited 9 time in scopus
Authors
Park, H. J.; Kim, H. J.; Kwon, H. J.; Lee, J. Y.; Cho, B. K.; Lee, W. J.; Yang, Y.; Cho, D. H.
Issue Date
2006-07-18
Publisher
Wiley-Blackwell
Citation
Exp Dermatol. 2006 Aug;15(8):589-95.
Keywords
AnimalsCells, Cultured*Down-RegulationErythema/metabolismDinoprostone/metabolismHumansInflammationInterleukin-18/*biosynthesis/metabolismKeratinocytes/metabolismMAP Kinase Signaling SystemMiceSkin/metabolism/pathologyTannins/*metabolismTime Factors*Ultraviolet Rays
Abstract
Tannic acids (TAs) are believed to be the key active components in plants, and are believed to be responsible for their anti-inflammatory, anti-viral effects and chemoprevention of cancer. However, the molecular mechanisms for the action of TA are unclear. This study examined the effects of TA on cutaneous inflammation with a human keratinocyte cell line (HaCaT). Interleukin-18 (IL-18) has multiple effects upon various cells involved in inflammatory response. In this study, the IL-18 mRNA expression and protein levels were reduced by a TA pretreatment. UV radiation can trigger the induction of the p38 mitogen-activated protein kinase (MAPK)-dependent signalling cascade. Immunoprecipitation and Western blot analysis was performed to determine if TA regulate the MAPK signalling pathway. TA significantly inhibited the activation of p38 MAPK and extracellular signal-regulated protein kinases. Moreover, TA-inhibited UVB enhanced the expression of the inflammatory mediators, IL-1, IL-6, tumor necrotic factor-alpha, cyclooxygenase-2 and prostaglandin E(2) in UVB-irradiated HaCaT cells. The topical application of TA on mouse skin treated with UVB irradiation has shown that TA inhibited the formation of erythema. These findings suggest that TA has significant anti-inflammatory effects on the UVB-induced response on the skin and may be a candidate natural compound for the regulation of cutaneous inflammation.
ISSN
0906-6705 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16842597

http://hdl.handle.net/10371/22837
DOI
https://doi.org/10.1111/j.1600-0625.2006.00449.x
Files in This Item:
There are no files associated with this item.
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Anatomy (해부학전공)Journal Papers (저널논문_해부학전공)
  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse