Impact of fenofibrate on NO and endothelial VCAM-1 expression in hyperlipidemic rats.
- Author:
Jun WU
1
;
Ming SUN
;
Jin-chao LIN
;
Zhao-chu HE
;
Bi-ru OU
;
Hai-sen GUO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Atherosclerosis; prevention & control; Cell Adhesion; Endothelium, Vascular; drug effects; metabolism; Fenofibrate; pharmacology; Hyperlipidemias; drug therapy; metabolism; Inflammation; Leukocytes; cytology; Nitric Oxide; metabolism; Rats; Rats, Sprague-Dawley; Vascular Cell Adhesion Molecule-1; metabolism
- From: Journal of Southern Medical University 2007;27(12):1872-1874
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanism of hyperlipidemia- and imflammation-induced functional impairment of the endothelium.
METHODSThe experiment was conducted using 3 groups of rats fed for 20 weeks with standard chow (control group), high-fat diet and high-fat diet with daily fenofibrate treatment (10 mg/kg, starting since the fifth week), respectively. After 4 and 20 weeks of feeding, respectively, serum lipid level and NO concentration were measured in the rats, and the epithelial vascular cell adhesion molecule-1 (VCAM-1) expression and cell adhesiveness to the aortic endothelium were observed.
RESULTSCompared with the control group, the rats with hyperlipidemia induced by long-term high-fat diet feeding showed lower NO concentration and increased leukocyte accumulation on the endothelial surface, exhibiting also stronger and more extensive endothelial expression of VCAM-1. In contrast, the hyperlipidemic rats with fenofibrate treatment shoed significantly decreased VCAM-1 expression and leukocyte adhesion with recovery of the NO level.
CONCLUSIONNO deficiency and activation of inflammation are involved in vascular impairment in rats with high-fat diet-induced hyperlipidemia, and fenofibrate can effectively prevent atherosclerosis by restoring NO concentration and down-regulating VCAM-1 expression in these rats.