RT Journal Article
SR Electronic
T1 Green Tea Inhibits Human Inducible Nitric-Oxide Synthase Expression by Down-Regulating Signal Transducer and Activator of Transcription-1α Activation
JF Molecular Pharmacology
JO Mol Pharmacol
FD American Society for Pharmacology and Experimental Therapeutics
SP 111
OP 120
DO 10.1124/mol.65.1.111
VO 65
IS 1
A1 Elisa Tedeschi
A1 Marta Menegazzi
A1 Ying Yao
A1 Hisanori Suzuki
A1 Ulrich Förstermann
A1 Hartmut Kleinert
YR 2004
UL http://molpharm.aspetjournals.org/content/65/1/111.abstract
AB Green tea has been reported to show anti-inflammatory properties because of its inhibitory effects on the expression of several pro-inflammatory genes. Because the inducible nitricoxide synthase (iNOS) plays an important role in chronic inflammatory diseases, we have focused our attention on the regulation of iNOS expression by green tea in two different human epithelial cell lines, alveolar A549/8 and colon DLD-1 cells. With the use of electrophoretic mobility shift assays, we found a green tea-mediated down-regulation of the DNA binding activity of the transcription factor signal transducer and activator of transcription-1α (STAT-1α), but not of nuclear factor-κB. This down-regulation of the STAT-1α DNA binding was shown to result from reduced tyrosine phosphorylation of the STAT-1α protein and not from antioxidative effects of the green tea extract. Green tea extract inhibited human iNOS expression in a concentration-dependent manner, quantified in terms of iNOS mRNA, iNOS protein, and nitric oxide production in both cell lines. This inhibitory effect of green tea resulted from transcriptional inhibition as shown in reporter gene experiments. These data suggest that green tea extracts may be promising at least as an auxiliary anti-inflammatory principle in chronic inflammatory diseases.