title: [Rosiglitazone inhibits atherosclerosis in apolipoprotein E-knockout mice].
abstract: OBJECTIVE
  To study the effect of rosiglitazone on atherosclerosis and potential mechanism in ApoE-knockout mice.
  
  
  METHODS
  Thirty-two 6-week-old ApoE-knockout mice were used as atherosclerosis model in two groups: rosiglitazone group (n = 18) and control group (n = 14). Each group contained equal numbers of male and female mice. All mice were fed with normal chow diet. In addition to normal diet, rosiglitazone group received rosiglitazone 17 mg/kg of body weight/day. Venous bloods were collected for plasma glucose and lipid analysis, and aorta were prepared for morphologic and immunohistochemical analysis after 14 weeks. Aortic root (1 cm) was cut and prepared for paraffin slice. The histomorphometric analysis of atherosclerotic lesion was performed by means of HE; positive percentage of macrophage cell and tumor necrosis factor-alpha were measured by means of immunohistochemistry in cross section. The ratio of lesion/aortic wall surface in the rest aorta was measured by means of Sudan IV staining in longitudinal section.
  
  
  RESULTS
  The amount of fatty streak in rosiglitazone group was significantly greater than that of control group; the gross number of lesions and the number of fibrous plaque and atheromatous plaque were similar in two groups. There were no differences in percentage of lesions in cross section in two groups. Rosiglitazone could significantly reduce the extend of atherosclerosis of longitudinal section, decrease the amount of macrophage cell and the level of tumor necrosis factor-alpha in lesions. The plasma glucose was normal and similar in two groups, and total cholesterol, LDL-cholesterol and triglyceride were significantly higher in rosiglitazone group.
  
  
  CONCLUSIONS
  Rosiglitazone suppresses the expression of tumor necrosis factor-alpha, reduces the number of macrophage cell in lesion, and inhibits the development of atherosclerosis.
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital University of Medical Science, Beijing 100029, China. zhaoqm123@sohu.com
authors.forename: Quan-ming
authors.initials: QM
authors.lastname: Zhao
authors.forename: Dong
authors.initials: D
authors.lastname: Yan
authors.forename: Ai-li
authors.initials: AL
authors.lastname: Song
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Qiang
authors.initials: Q
authors.lastname: Shi
authors.forename: Lü-ya
authors.initials: LY
authors.lastname: Wang
authors.forename: Dong
authors.initials: D
authors.lastname: Chen
authors.forename: Wei
authors.initials: W
authors.lastname: Fang
authors.forename: Ying
authors.initials: Y
authors.lastname: Wu
authors.forename: Jin-peng
authors.initials: JP
authors.lastname: Xu
authors.forename: Xin
authors.initials: X
authors.lastname: Chen
authors.forename: Tie-jun
authors.initials: TJ
authors.lastname: Chen
authors.forename: Shu-hua
authors.initials: SH
authors.lastname: Mi
authors.forename: Shu-zheng
authors.initials: SZ
authors.lastname: Lü
mesh_terms: D000818:Animals; D001011:Aorta / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics / Q000502:physiology*; D050197:Atherosclerosis / Q000097:blood / Q000473:pathology / Q000517:prevention & control*; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight / Q000187:drug effects; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D008264:Macrophages / Q000473:pathology; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D000077154:Rosiglitazone; D045162:Thiazolidinediones / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D001057:Apolipoproteins E; D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D007004:Hypoglycemic Agents; D045162:Thiazolidinediones; D014409:Tumor Necrosis Factor-alpha; D000077154:Rosiglitazone