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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-1-5
pubmed:abstractText
Accumulating evidence suggests that statins have beneficial effects which are independent of their lipid-lowering actions, on vascular cells. Here, we investigated whether the HMG-CoA reductase inhibitor rosuvastatin can inhibit atherosclerotic lesion development with favorable effects on endothelial cells in ApoE-deficient mice. Rosuvastatin rapidly phosphorylated Akt and endothelial nitric oxide synthase (eNOS) in human endothelial cells. Endothelial cell death induced by serum starvation was significantly inhibited by rosuvastatin (percent cell death; 45.9+/-2.4% vs. 37.3+/-1.1%, p<0.05). Eight-week-old ApoE-deficient mice were orally administered vehicle or rosuvastatin at a dose of 20mg/kg/day for 24 weeks. There was no significant difference in cholesterol profile. Rosuvastatin preserved endothelial lining at the aortic root (CD31-positive luminal side; 63.8+/-2.8% vs. 81.7+/-3.9%, p<0.05). En face Sudan IV staining of aorta revealed that rosuvastatin significantly decreased the atherosclerotic area (21.9+/-2.9% vs. 11.9+/-1.9%, p<0.05). Lipid deposition at the atherosclerotic area was also suppressed by rosuvastatin with more stabilized morphologic features as determined by oil red O staining (3.4+/-0.4% vs. 1.7+/-0.4%, p<0.05). Our findings indicate that rosuvastatin protects endothelial cells from death with phosphorylation of Akt and eNOS. These effects may contribute, at least in part, to the anti-atherosclerotic effects of rosuvastatin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1950-6007
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
19-26
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Rosuvastatin prevents endothelial cell death and reduces atherosclerotic lesion formation in ApoE-deficient mice.
pubmed:affiliation
Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't