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Inhibitory effects of triphlorethol-A on MMP-1 induced by oxidative stress in human keratinocytes via ERK and AP-1 inhibition

Cited 19 time in Web of Science Cited 18 time in Scopus
Authors
Kang, Kyoung Ah; Zhang, Rui; Piao, Mei Jing; Ko, Dong Ok; Wang, Zhi Hong; Lee, Kyung; Kim, Bum Joon; Shin, Taekyun; Park, Jae Woo; Lee, Nam Ho; Yoo, Byoung Sam; Hyun, Jin Won
Issue Date
2008-06-24
Publisher
Taylor & Francis
Citation
J Toxicol Environ Health A. 71(15):992-999
Keywords
Blotting, WesternCatalase/metabolismCell Survival/drug effectsCells, CulturedComet AssayDNA/drug effectsDNA DamageEnzyme InductionExtracellular Signal-Regulated MAP Kinases/*antagonists & inhibitorsFluorescent Antibody Technique, IndirectFree Radical Scavengers/*pharmacologyHumansHydrogen Peroxide/pharmacologyKeratinocytes/*drug effects/enzymologyMatrix Metalloproteinase 1Oxidants/pharmacologyOxidative StressPhloroglucinol/*analogs & derivatives/pharmacologyTranscription Factor AP-1/*antagonists & inhibitors
Abstract
Oxidative stress is known to generate reactive oxygen species (ROS) in cells, which subsequently induce the synthesis of matrix metalloproteinases (MMP) and an aging phenomenon. The protective effects of triphlorethol-A, derived from Ecklonia cava, were investigated against hydrogen peroxide (H(2)O(2))-induced damage using human skin keratinocytes. Data showed that triphlorethol-A inhibited ROS formation, induced catalase expression, inhibited DNA damage, and increased cell viability in keratinocytes. Triphlorethol-A treatment significantly reduced MMP-1 expression and production, compared to H(2)O(2)-treated cells. In addition, triphlorethol-A abrogated the activation of extracellular signal regulated protein kinase (ERK), which originates upstream of MMP-1 expression, and was induced by H(2)O(2) treatment. Moreover, triphlorethol-A inhibited DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of ERK. Data indicate that the antioxidative properties of triphlorethol-A involve the inhibition of MMP-1 via ERK and AP-1 inhibition.
ISSN
1528-7394 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18569608

http://pdfserve.informaworld.com/271715_758494928_794223963.pdf

http://hdl.handle.net/10371/67886
DOI
https://doi.org/10.1080/01932690801934653
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College of Medicine/School of Medicine (의과대학/대학원)Microbiology (미생물학전공)Journal Papers (저널논문_미생물학전공)
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