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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: Epigallocatechin gallate-mediated protection against tumor necrosis factor-α-induced monocyte chemoattractant protein-1 expression is heme oxygenase-1 dependent.

Authors: Zheng, Yuanyuan; Toborek, Michal; Hennig, Bernhard

Published In Metabolism, (2010 Oct)

Abstract: Flavonoids have been suggested to protect against atherosclerosis via their antioxidant and anti-inflammatory properties. Heme oxygenase-1 (HO-1) is an enzyme that plays an important role in the vascular system, and its induction may provide a protective role against atherosclerosis. We hypothesize that flavonoids can down-regulate endothelial inflammatory parameters by modulating HO-1-regulated cell signaling. We focused on the role of HO-1 and its major metabolic product, bilirubin, on mechanisms of tumor necrosis factor-α-induced endothelial cell activation and protection by the catechin epigallocatechin gallate (EGCG). Pretreatment with EGCG inhibited the secretion of monocyte chemoattractant protein-1 and the activation of activator protein-1 in porcine aortic endothelial cells stimulated with tumor necrosis factor-α. Moreover, EGCG up-regulated the expression of HO-1 and further induced the secretion of bilirubin. The observed anti-inflammatory effects of EGCG were mimicked by the HO-1 inducer cobalt protoporphyrin and abolished by HO-1 gene silencing. These data suggest that the protective properties of flavonoids, such as EGCG, against endothelial inflammation may be regulated in part though induction of HO-1 and subsequent activator protein-1 signaling.

PubMed ID: 20580034 Exiting the NIEHS site

MeSH Terms: Animals; Bilirubin/metabolism; Bilirubin/pharmacology; Catechin/analogs & derivatives*; Catechin/pharmacology; Cells, Cultured; Chemokine CCL2/antagonists & inhibitors; Chemokine CCL2/genetics*; Cytoprotection/drug effects*; Cytoprotection/genetics; Endothelial Cells/drug effects; Endothelial Cells/metabolism; Gene Expression/drug effects; Heme Oxygenase-1/antagonists & inhibitors; Heme Oxygenase-1/genetics; Heme Oxygenase-1/physiology*; Inflammation/genetics; Inflammation/metabolism; Inflammation/prevention & control; Oligodeoxyribonucleotides, Antisense/pharmacology; Swine; Transfection; Tumor Necrosis Factor-alpha/pharmacology*; Up-Regulation/drug effects

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