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Chronic administration of low dose EGCG inhibits TNF‐α‐induced IL‐6 and IL‐8 production in rheumatoid arthritis synovial fibroblasts
Author(s) -
Riegsecker Sharayah,
Ahmed Salahuddin
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.643.18
Subject(s) - rheumatoid arthritis , tumor necrosis factor alpha , medicine , protein kinase b , mapk/erk pathway , pharmacology , stimulation , p38 mitogen activated protein kinases , proinflammatory cytokine , fibroblast , arthritis , immunology , cancer research , inflammation , endocrinology , phosphorylation , chemistry , biochemistry , in vitro
Rheumatoid arthritis (RA) is a chronic inflammatory disease in which cytokines stimulate synovial fibroblast proliferation leading to the destruction of the joints. In this study we evaluated the efficacy of chronic low doses of epigallocatechin‐3‐gallate (EGCG), a polyphenol found in green tea, in regulating TNF‐α‐induced IL‐6 and and IL‐8 production. RA snyovial fibroblasts were treated with chronic low doses of EGCG (100–1000 nM) for 7 days followed by TNF‐α stimulation. Conditioned medium was used for the quantification of IL‐6 and IL‐8 by ELISA and cell lysates were prepared for the analysis of signaling proteins. Chronic administration of EGCG inhibited the ability of TNF‐α to induce IL‐6 and IL‐8 production in RA synovial fibroblasts in a dose‐dependent manner(p<0.05). Evaluation of the signaling pathways by Western blotting revealed that chronic exposure of EGCG selectively inhibited TNF‐α‐induced phosphorylation of JNK p54 and AKT, with no or little effect on p‐ERK or p‐P38 MAPKs. These results suggest that the chronic consumption of EGCG, which can be achieved physiologically by drinking green tea, has an ability to decrease the inflammatory millieu and consequently limit joint damage in RA. Grant Funding Source : NIH