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Flavonoids protect against endothelial dysfunction by induction of heme oxygenase‐1
Author(s) -
Zheng Yuanyuan,
Oesterling Elizabeth,
Toborek Michal,
Hennig Bernhard
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.717.11
Subject(s) - heme oxygenase , oxidative stress , inflammation , chemistry , pharmacology , endothelial dysfunction , heme , biochemistry , medicine , enzyme , immunology
Flavonoids have been suggested to protect against atherosclerosis by their anti‐oxidant and anti‐inflammatory properties. Little is known about the mechanisms and flavonoids structures required for prevention against endothelial cell dysfunction in the development of atherosclerosis. Heme oxygenase (HO‐1) is an enzyme that plays an important role in protecting against endothelial cell oxidative stress and inflammation. We hypothesize that flavonoids with specific structures protect against endothelial cell inflammation by induction of HO‐1. We found that the 2, 3‐double bond, 4‐keto group and 3‐hydroxyl group of the C‐ring are the main structure requirements for the induction of HO‐1. Flavonoids with these chemical structures, such as epigallocatechin gallate (EGCG), quercetin, and galangin up‐regulated the expression of HO‐1, and protected against hydrogen peroxide‐induced oxidative stress as well as TNF‐α‐induced prostaglandin PGE‐2 expression. These protective effects were partially blocked by pre‐treatment with tin‐protoporphyrin IX, the inhibitor of HO‐1. These data suggested that the protective effects of specific flavonoids against oxidative stress and inflammation are regulated through induction of HO‐1. These data add to nutritional recommendations for optimal cardiovascular health. (Supported by grants from NIEHS, NIH (P42ES07380) and the University of Kentucky AES).