title: Aspirin inhibits fractalkine expression in atherosclerotic plaques and reduces atherosclerosis in ApoE gene knockout mice.
abstract: OBJECTIVE
  To determine the fractalkine expression in the aorta of ApoE (-/-) mice and the effect of high-dose aspirin intervention on fractalkine expression and atherosclerotic lesion formation.
  
  
  METHODS
  Twenty-one male ApoE gene knockout mice were randomized into three groups to receive either placebo in addition to normal mice chow (n = 7), placebo in addition to a high-fat diet (n = 7), or aspirin (58 mg/kg/d) in addition to a high-fat diet (n = 7). After 12 weeks of study, the mice were euthanized and serum cholesterol, thromboxane B(2), and 6-keto-PGF(1alpha) were examined. Fractalkine and cyclooxygenase expression in aorta were measured and the atherosclerotic lesion analyzed.
  
  
  RESULTS
  Pathology image analysis showed that the atherosclerotic plaque was the most extensive in the high-fat diet group while the addition of aspirin greatly reduced the severity of the plaque. Both RT-PCR analysis and immunohistochemical analysis showed that fractalkine expression was the strongest in the high-fat diet group and was significantly decreased by aspirin treatment. Serum thromboxane B(2) was lowered by aspirin while 6-keto-PGF(1alpha) and cholesterol remained unchanged.
  
  
  CONCLUSIONS
  The results of our study indicate that high dose aspirin can improve the atherosclerotic lesion and suppress the fractalkine expression in murine aorta.
authors.affiliation: Department of Geriatrics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China. katharinehong@163.com
authors.forename: Hong
authors.initials: H
authors.lastname: Liu
authors.forename: Deqian
authors.initials: D
authors.lastname: Jiang
authors.forename: Shebing
authors.initials: S
authors.lastname: Zhang
authors.forename: Baiqing
authors.initials: B
authors.lastname: Ou
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics*; D001241:Aspirin / Q000494:pharmacology* / Q000627:therapeutic use; D050197:Atherosclerosis / Q000097:blood / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D002097:C-Reactive Protein / Q000378:metabolism; D054428:Chemokine CX3CL1 / Q000235:genetics / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood; D051545:Cyclooxygenase 1 / Q000235:genetics / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D004041:Dietary Fats / Q000008:administration & dosage; D015870:Gene Expression / Q000187:drug effects*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D011460:Prostaglandins F / Q000097:blood; D013929:Thromboxane B2 / Q000097:blood; D014280:Triglycerides / Q000097:blood
chemical_list: D001057:Apolipoproteins E; D054428:Chemokine CX3CL1; C515539:Cx3cl1 protein, mouse; D004041:Dietary Fats; D008565:Membrane Proteins; D011460:Prostaglandins F; D014280:Triglycerides; D013929:Thromboxane B2; D002097:C-Reactive Protein; D002784:Cholesterol; C077623:Ptgs2 protein, mouse; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496512:Ptgs1 protein, mouse; D001241:Aspirin; C100006:prostaglandin F1