Epigallocatechin-3-Gallate Suppresses the Expression of TNF-α-Induced MMP-1 via MAPK / ERK Signaling Pathways in Human Dermal Fibroblasts

Deeper wrinkles and loss of elasticity are one of the skin-aging symptoms. Collagen breakdown by matrix metalloproteinase-1 (MMP-1), which is induced by reactive oxygen species (ROS) and pro-inflammatory cytokines, has been known to be responsible for these skin-aging symptoms. Therefore, much atten...

Full description

Saved in:
Bibliographic Details
Published inBiological and Pharmaceutical Bulletin Vol. 44; no. 1; pp. 18 - 24
Main Authors Hea-Ryeoun Wona, Pyeongjae Leeb, Sol-ra Oha, Yong-Min Kima
Format Journal Article
LanguageJapanese
Published Pharmaceutical Society of Japan 01.01.2021
Online AccessGet full text

Cover

Loading…
More Information
Summary:Deeper wrinkles and loss of elasticity are one of the skin-aging symptoms. Collagen breakdown by matrix metalloproteinase-1 (MMP-1), which is induced by reactive oxygen species (ROS) and pro-inflammatory cytokines, has been known to be responsible for these skin-aging symptoms. Therefore, much attention has been paid to chemicals to suppress the MMP-1 activity. Epigallocatechin-3-gallate (EGCG), catechin rich in green tea, has been reported to show antioxidant and protect skin from various stimuli such as UV and chemicals. In this study, we evaluated the inhibitory effect of EGCG on MMP-1 gene expression and secretion in tumor necrosis factor-α (TNF-α)-treated human dermal fibroblast cells (Hs68 cells). Pre-treatment with EGCG (10 and 20μM) suppressed TNF-1α-induced MMP-1 expression and secretion. EGCG also reduced the phosphorylation of extracellular signal regulated kinase (ERK) significantly but not that of p38 activation and c-Jun N-terminal kinase (JNK). Besides, EGCG (10 and 20μM) showed the inhibitory effect on mitogen-activated protein extracellular kinase (MEK) and Src phosphorylation which is reported to be upstream signal proteins of ERK signal pathway. Based on these results, EGCG might have potential activity to slow down the skin-aging through inhibition of collagen breakdown, which remains to be elucidated.
ISSN:0918-6158
1347-5215