Eupatilin with PPAR alpha agonistic effects inhibits TNF alpha-induced MMP signaling in HaCaT cells
DC Field | Value | Language |
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dc.contributor.author | Jung, Yujung | - |
dc.contributor.author | Kim, Jin-Chul | - |
dc.contributor.author | Choi, Yongsoo | - |
dc.contributor.author | Lee, Sullim | - |
dc.contributor.author | Kang, Ki Sung | - |
dc.contributor.author | Kim, Yong Kee | - |
dc.contributor.author | Kim, Su-Nam | - |
dc.date.available | 2020-02-27T16:42:41Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2017-11-04 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/5470 | - |
dc.description.abstract | Eupatilin (5,7-dihydroxy-3,4,6-trimethoxyflavone) is a flavonoid compound exhibiting several beneficial biological activities, including neuroprotection, anti-cancer, antinociception, chondroprotection, anti oxidation, and anti-inflammation. Our previous study demonstrated that eupatilin specifically activates peroxisome proliferator-activated receptor alpha (PPAR alpha) through direct binding. The PPAR subfamily includes ligand-dependent transcription factors that consist of three isotypes: PPAR alpha, PPAR beta/delta, and PPAR gamma. All isotypes are involved in inflammation, epidermal proliferation/differentiation and skin barrier function. Among them, PPAR alpha regulates lipid and glucose metabolism and skin homeostasis. In this study, we confirm that the ability of eupatilin as a PPAR alpha activator significantly inhibited tumor necrosis factor-alpha (TNF alpha)-induced matrix metalloproteinase (MMP)-2/-9 expression and proteolytic activity in HaCaT human epidermal keratinocytes. Furthermore, we found that eupatilin subsequently suppressed I kappa B alpha phosphorylation, blocked NF-kappa B p65 nuclear translocation and down-regulated MAPK/AP-1 signaling via PPAR alpha activation. Taken together, our data suggest that eupatilin inhibits TNF alpha-induced MMP-2/-9 expression by suppressing NF-kappa B and MAPK/AP-1 pathways via PPAR alpha. Our findings suggest the usefulness of eupatilin for preventing skin aging. (C) 2017 Elsevier Inc. All rights reserved. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.relation.isPartOf | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.subject | FACTOR-KAPPA-B | - |
dc.subject | SKIN IN-VIVO | - |
dc.subject | MATRIX-METALLOPROTEINASE | - |
dc.subject | ACTIVATION | - |
dc.subject | TRANSCRIPTION | - |
dc.subject | GENE | - |
dc.subject | KERATINOCYTES | - |
dc.subject | INFLAMMATION | - |
dc.subject | EXPRESSION | - |
dc.subject | PATHWAYS | - |
dc.title | Eupatilin with PPAR alpha agonistic effects inhibits TNF alpha-induced MMP signaling in HaCaT cells | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000413134200035 | - |
dc.identifier.doi | 10.1016/j.bbrc.2017.09.043 | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.493, no.1, pp.220 - 226 | - |
dc.identifier.scopusid | 2-s2.0-85029213520 | - |
dc.citation.endPage | 226 | - |
dc.citation.startPage | 220 | - |
dc.citation.title | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.volume | 493 | - |
dc.citation.number | 1 | - |
dc.contributor.affiliatedAuthor | Kang, Ki Sung | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Eupatilin | - |
dc.subject.keywordAuthor | PPAR alpha | - |
dc.subject.keywordAuthor | MMPs | - |
dc.subject.keywordAuthor | NF-kappa B | - |
dc.subject.keywordAuthor | AP-1 | - |
dc.subject.keywordPlus | FACTOR-KAPPA-B | - |
dc.subject.keywordPlus | SKIN IN-VIVO | - |
dc.subject.keywordPlus | MATRIX-METALLOPROTEINASE | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | TRANSCRIPTION | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | KERATINOCYTES | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PATHWAYS | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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