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Sodium Ferulate Modified Gene Expression Profile of Oxidized Low-Density Lipoprotein-Stimulated Human Umbilical Vein Endothelial Cells
Dongxian Zhang, MD1,
Zhuoyue Bi, MD2*,
Yang Li, MD, PhD3,
Hong Zheng, MD4,
Li Li, MD5,
Jingping Ouyang, MD6,
Baohua Wang, MD, PhD6,
and
Yongyi Bi, MD, PhD5
1 School of Public Health, Wuhan University, Wuhan, Hubei, PR China; Nanyang Medical College, Henan, PR China
2 School of Pharmacy, Wuhan University, Wuhan, PR China
3 Hubei Provincial Center for Disease Control and Prevention, Wuhan, PR China
4 School of Basic Medical Science, Yunyang Medical College, Hubei, PR China
5 School of Public Health, Wuhan University, Wuhan, Hubei, PR China
6 Department of Pathology and Pathophysiology, School of Medicine, Wuhan University, Wuhan, PR China
* To whom correspondence should be addressed. E-mail: bizhuoyue{at}yahoo.cn.
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Abstract |
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Oxidized low-density lipoprotein (ox-LDL) is known to trigger vascular injury in atherosclerosis development. Sodium ferulate is an effective component from Chinese medicines with various beneficial cardiovascular pharmacological activities. Here, we investigated the effects of sodium ferulate on the gene expression profile of ox-LDL-stimulated endothelial cells. Cultured human umbilical vein endothelial cells (HUVECs) were treated with ox-LDL (50 μg/mL) in the absence or presence of sodium ferulate (5 μmol/L). Sodium ferulate significantly reduced ox-LDL-induced endothelial cell death as evaluated by cell viability assay. Human oligonucleotide microarray analysis demonstrated that a total of 32 ox-LDL-induced genes were significantly downregulated to control levels by sodium ferulate. These genes included members from families of chemokine, inflammatory factor, growth factor, and nuclear receptor. These data provided an overview of the gene expression profile of endothelial cells in response to ox-LDL and sodium ferulate, and demonstrated that sodium ferulate could regulate the expression of inflammation-related genes in endothelial cells and has the potential to benefit endothelial function in the setting of atherosclerosis.
First published on October 16, 2009, doi:10.1177/1074248409347986
Journal of Cardiovascular Pharmacology and Therapeutics 2009;14:302.
A more recent version of this article appeared on December 1, 2009

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