Rosuvastatin attenuates vascular endothelial adhesiveness in apolipoprotein E-deficient mice.
- Author:
Wei LI
1
;
Hai-ying HUANG
;
Zhi-yong WU
;
Fang-qiu XIE
;
Xu-ri ZHANG
;
Pin GUAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apolipoproteins E; genetics; Cell Adhesion; drug effects; Endothelium, Vascular; cytology; Fluorobenzenes; pharmacology; Mice; Mice, Inbred C57BL; Mice, Knockout; Monocytes; drug effects; metabolism; Pyrimidines; pharmacology; Rosuvastatin Calcium; Sulfonamides; pharmacology; Vascular Cell Adhesion Molecule-1; metabolism
- From: Chinese Journal of Cardiology 2009;37(1):69-72
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the anti-inflammatory effects on the vessel wall of rosuvastatin in apolipoprotein E-deficient mice.
METHODSEight-week-old apolipoprotein E-deficient mice fed a normal chow diet were treated with vehicle or various doses of rosuvastatin (1, 5, or 20 mg/kg) by subcutaneous injection for 2 or 6 weeks prior to sacrifice. Endothelial adhesiveness for monocytes was determined by functional binding assay. The expressions of vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 in the vessel wall were detected by quantitative real-time polymerase chain reaction.
RESULTSEndothelial adhesiveness for monocytes was significantly attenuated after 2 or 6 weeks treatments with 5 or 20 mg/kg rosuvastatin. Rosuvastatin also significantly reduced the expressions of vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 in the vessel wall.
CONCLUSIONThe anti-inflammatory effects of suvastatin might be responsible for attenuating the pathogenesis of atherogenesis in apolipoprotein E-deficient mice.