title: No effect of cyclooxygenase inhibition on plaque size in atherosclerosis-prone mice.
abstract: OBJECTIVE
  To study the role of cyclooxygenase (COX) inhibition on the development of advanced atherosclerosis in apolipoprotein E-deficient (apoE(-/-)) mice.
  
  
  METHODS
  Sixty apoE(-/-) mice were divided into three groups: a control group, a group fed standard mouse chow supplemented with 0.0067% (wt/wt) MF Tricyclic (selective COX-2 inhibitor), and a group fed the diet supplemented with 0.0134% (wt/wt) sulindac (non-selective COX inhibitor). Four months later, the mice were killed and the atherosclerotic plaque area in the aortic root was measured.
  
  
  RESULTS
  Mean body weights did not differ at any time. The MF Tricyclic and sulindac groups had drug plasma levels of 1.31 +/- 0.11 and 0.84 +/- 0.23 micro g/ml, respectively. Plasma total cholesterol and triglyceride values were similar in all three groups. A small difference in plasma levels of high-density lipoprotein cholesterol was found between the groups (p = 0.03). Advanced atherosclerotic plaques were present in mice from all three groups, but there was no difference in mean plaque size between the groups (p = 0.9).
  
  
  CONCLUSIONS
  Neither selective COX-2 nor non-selective COX inhibition influenced the development of advanced atherosclerosis in apoE(-/-) mice.
authors.affiliation: Department of Cardiology, Institute of Experimental Clinical Research, Aarhus University Hospital (Skejby), DK-8200 Aarhus N, Denmark.
authors.forename: Mette
authors.initials: M
authors.lastname: Olesen
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Kwong
authors.forename: Arguello
authors.initials: A
authors.lastname: Meztli
authors.forename: Frederic
authors.initials: F
authors.lastname: Kontny
authors.forename: Ingebjörg
authors.initials: I
authors.lastname: Seljeflot
authors.forename: Harald
authors.initials: H
authors.lastname: Arnesen
authors.forename: Line
authors.initials: L
authors.lastname: Lyngdorf
authors.forename: Erling
authors.initials: E
authors.lastname: Falk
mesh_terms: D000465:Algorithms; D000704:Analysis of Variance; D000818:Animals; D001013:Aorta, Thoracic / Q000473:pathology; D001018:Aortic Diseases / Q000209:etiology / Q000473:pathology*; D001057:Apolipoproteins E / Q000172:deficiency*; D001161:Arteriosclerosis / Q000209:etiology / Q000473:pathology*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology*; D004195:Disease Models, Animal; D005663:Furans / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D013467:Sulindac / Q000494:pharmacology
chemical_list: D001057:Apolipoproteins E; D016861:Cyclooxygenase Inhibitors; D005663:Furans; C102563:3-(3,4-difluorophenyl)-4-(4-(methylsulfonyl)phenyl)-2(5H)-furanone; D013467:Sulindac