Resveratrol and its metabolites modulate cytokine-mediated induction of eotaxin-1 in human pulmonary artery endothelial cells.

Coronary heart disease (CHD) is a leading cause of death in many developed countries. Evidence has long implicated endothelial injury and inflammation as apical events in the pathogenesis of atherosclerosis, the primary cause of CHD. Numerous risk factors contribute to a damaged, inflamed endothelium. Conversely, cardioprotective agents targeting the dysfunctional endothelium have also been identified, notably from dietary sources. We have used cultured human pulmonary artery endothelial cells (HPAECs) to test the diet-mediated cardioprotective hypothesis. In this review, we summarize our recent findings on control of transcription and expression of inflammation biomarker eotaxin-1 in HPAECs exposed to single or combined proinflammatory cytokines interleukin-13 (IL-13) and tumor necrosis factor-α (TNF-α), and attenuation of the observed eotaxin-1 responses by prior or simultaneous treatment with resveratrol and its metabolites. Control of eotaxin-1 gene regulation may be considered an in vitro model to evaluate agents linking cardioprotection with endothelial cell damage and inflammation.