Epigallocatechin-3-gallate suppresses TNF-[alpha] -induced production of MMP-1 and -3 in rheumatoid arthritis synovial fibroblasts

Rheumatoid arthritis (RA) synovial fibroblasts produce matrix metaloproteinases (MMPs), which destruct cartilage and bone in RA joint. Tumor necrosis factor-α (TNF-α) is one of the most important mediator leading to MMP production in RA synovial fibroblasts. Here we show that epigallocatechin-3-Gall...

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Bibliographic Details
Published in:Rheumatology international 2008-11, Vol.29 (1), p.23
Main Authors: Yun, Hee-jin, Yoo, Wan-hee, Han, Myung-kwan, Lee, Young-rae, Kim, Jong-suk, Lee, Sang-il
Format: Article
Language:English
Subjects:
Kinases
Rheumatoid arthritis
Online Access:Get full text
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Summary:Rheumatoid arthritis (RA) synovial fibroblasts produce matrix metaloproteinases (MMPs), which destruct cartilage and bone in RA joint. Tumor necrosis factor-α (TNF-α) is one of the most important mediator leading to MMP production in RA synovial fibroblasts. Here we show that epigallocatechin-3-Gallate (EGCG) suppresses TNF-α-induced production of MMP-1 and MMP-3 in RA synovial fibroblasts, which was accompanied by inhibition of mitogen activated protein kinase (MAPK) and activator protein-1 (AP-1) pathways. EGCG treatment resulted in dose-dependent inhibition of TNF-α-induced production of MMP-1 and MMP-3 at the protein and mRNA levels in RA synovial fibroblast. EGCG treatment also inhibited TNF-α-induced phosphorylation of MAPKs, such as ERK1/2, p38, JNK. Electrophoretic mobility shift assay revealed that EGCG inhibits binding of AP-1 proteins to its response elements in synovial fibroblast treated. Thus, EGCG may play a role in regulating inflammation and bone destruction in RA patients.[PUBLICATION ABSTRACT]
ISSN:0172-8172
1437-160X
DOI:10.1007/s00296-008-0597-5