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Quercitrin inhibits oxidized LDL‐induced expression of scavenger receptors and vascular endothelial growth factor in cultured murine macrophages
Author(s) -
Choi JungSuk,
Kang YoungHee
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.563.33
Subject(s) - quercitrin , scavenger receptor , chemistry , foam cell , apoptosis , receptor , macrophage , microbiology and biotechnology , vascular endothelial growth factor , cancer research , biochemistry , biology , quercetin , lipoprotein , cholesterol , antioxidant , vegf receptors , in vitro
Oxidized LDL (oxLDL) has been implicated in the pathogenesis of atherosclerosis accompanying lipid accumulation, pro‐inflammatory responses, and apoptotic endothelial cell death. One pro‐atherogenic mechanism of oxidized LDL involves local up‐regulation of pro‐inflammatory mediators such as vascular endothelial growth factor (VEGF). We examined the ability of polyphenoric quercitrin to inhibit oxLDL‐induced macrophage foam cell formation via class A scavenger receptors (SR‐A). Murine macrophages J774A.1 were cultured with 10 µg/ml oxLDL for 4 h in the presence of 10 µM quercitrin. Submicromolar quercitrin blocked apoptotic cell death induced by cytotoxic oxLDL at 100 µg/ml and considerably lessened the oxLDL‐induced foam cell formation, evidenced by Oil Red O staining. Western blot analysis revealed that oxLDL up‐regulated SR‐A expression and VEGF, which was rapidly abolished by 10 µM quercitrin within 4 h. In addition, 10 µM quercitrin down‐regulated oxLDL‐induced activation of peroxisome proliferator‐activated receptor gamma (PPARγ). These results demonstrate that quercitrin dampens the expression of macrophage SR‐A and VEGF with blocking PPARγ activation. We conclude that quercitrin may be an anti‐atherogenic agent blocking foam cell formation pertaining to VEGF production. Supported by Brain Korea 21 from Korea Research Foundation.