Control of eotaxin-1 expression and release by resveratrol and its metabolites in culture human pulmonary artery endothelial cells.

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Yang CJ, Lin CY, Hsieh TC, Olson SC, Wu JM

Control of eotaxin-1 expression and release by resveratrol and its metabolites in culture human pulmonary artery endothelial cells.

Am J Cardiovasc Dis. 2011;1(1):16-30. Epub 2011 Apr 26.

PubMed ID
22254182 [ View in PubMed
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Abstract

Population studies suggest that moderate red wine intake correlates with reduced risk of cardiovascular disease (CVD); cardioprotection may attribute to consumption of red wine polyphenol resveratrol. Since inflammation plays a key role in CVD, we investigated modulation of inflammation by resveratrol and its metabolites by determining the expression and release of chemokine, eotaxin-1, in cultured human pulmonary artery endothelial cells (HPAEC) treated with proinflammatory cytokines IL-13 and TNF-alpha. Up-regulation of eotaxin-1 gene expression by IL-13 or TNF-alpha was confirmed by RT-PCR, by reporter assays using eotaxin-1 gene promoter constructs, and by the changes in transcriptional factors STAT6 and NF-kappaB. Exposure to resveratrol suppressed IL-13 and TNF-alpha induced eotaxin-1 gene expression as well as attenuated the eotaxin-1 promoter activity, in coordination with inhibition of expression of JAK-1, reduction in phosphorylated-STAT6 and decreased p65 subunit of NF-kappaB. In addition, quantitative determination of eotaxin-1 release using enzyme-linked immunosorbent assay (ELISA) showed increased eotaxin-1 release in response to treatment by IL-13 and TNF-alpha, which was effectively inhibited by resveratrol. Whether resveratrol metabolites affected eotaxin-1 was also tested; piceatannol showed potency similar to resveratrol. We propose that control of eotaxin-1 expression and release by proinflammatory cytokines in HPAEC may be considered as an in vitro model for screening and discovering polyphenols with anti-inflammatory activities and cardioprotective potentials.