Inflammation 2002,
PMID: 12238566
Chen, Philip C; Wheeler, Derek S; Malhotra, Vivek; Odoms, Kelli; Denenberg, Alvin G; Wong, Hector R
Interleukin-8 (IL-8) is a principle neutrophil chemoattractant and activator in humans. There is interest in developing novel pharmacological inhibitors of IL-8 gene expression as a means for modulating inflammation in disease states such as acute lung injury. Herein we determined the effects of epigallocatechin-3-gallate (EGCG), a green tea-derived polyphenol, on tumor necrosis factor-alpha (TNF-alpha)-mediated expression of the IL-8 gene in A549 cells. EGCG inhibited TNF-alpha-mediated IL-8 gene expression in a dose response manner, as measured by ELISA and Northern blot analysis. This effect appears to primarily involve inhibition of IL-8 transcription because EGCG inhibited TNF-alpha-mediated activation of the IL-8 promoter in cells transiently transfected with an IL-8 promoter-luciferase reporter plasmid. In addition, EGCG inhibited TNF-alpha-mediated activation of IkappaB kinase and subsequent activation of the IkappaB alpha/NF-kappaB pathway. We conclude that EGCG is a potent inhibitor of IL-8 gene expression in vitro. The proximal mechanism of this effect involves, in part, inhibition of IkappaB kinase activation.
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Text Mining Data
IL-8 → tumor necrosis factor-alpha (TNF-alpha): "
Herein we determined the effects of epigallocatechin-3-gallate ( EGCG ), a green tea derived polyphenol, on
tumor necrosis factor-alpha (TNF-alpha) mediated expression of the
IL-8 gene in A549 cells
"
IL-8 → TNF-alpha: "
EGCG inhibited TNF-alpha mediated IL-8 gene expression in a dose response manner, as measured by ELISA and Northern blot analysis
"
IL-8 → TNF-alpha: "
This effect appears to primarily involve inhibition of IL-8 transcription because EGCG inhibited TNF-alpha mediated activation of the IL-8 promoter in cells transiently transfected with an IL-8 promoter-luciferase reporter plasmid
"
IkappaB kinase → TNF-alpha: "
In addition, EGCG inhibited TNF-alpha mediated activation of IkappaB kinase and subsequent activation of the IkappaB alpha/NF-kappaB pathway
"
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