title: Effects of atorvastatin on expression of ICAM-1 in atherosclerotic rabbits.
abstract: OBJECTIVE
  Lipid accumulation and inflammatory response are major events in the progression of atherosclerosis. This research was performed to determine if atorvastatin could prevent atherosclerosis and its underlying mechanisms.
  
  
  METHODS
  An atherosclerotic model was established in rabbits. Atorvastatin was administrated by gavage. Blood samples were collected to measure plasma total cholesterol, total triglyceride and low-density lipoprotein (LDL)-cholesterol. After the high-cholesterol diet with or without atorvastatin treatment, the morphological changes of the rabbits were examined with hematoxylin and eosin staining of tissues, and the expression of intercellular adhesion molecule 1 (ICAM-1) was determined by immuno-staining and reverse transcriptase-PCR (RT-PCR).
  
  
  RESULTS
  Atorvastatin significantly reduced plasma levels of total cholesterol (41.7%) and LDL-cholesterol (34.6%). Neither the hypercholesterol diet nor atorvastatin treatment had any significant impact on body weight and plasma triglycerides. Treatment with atorvastatin significantly restored 40.9% of the widened intima and even down-regulated the ratio of intima/media by 55.5%. The inhibitory effects of atorvastatin on the expression of ICAM-1 showed a decrease of up to 37.6% (P < 0.01). The diseased rabbits showed a 167.3% increase in ICAM-1 mRNA expression (P < 0.01), which was reversed by nearly 46.4% by treatment with atorvastatin.
  
  
  CONCLUSIONS
  Atorvastatin significantly prevents atherosclerotic changes in rabbits with a high-cholesterol diet, possibly by lowering plasma lipids and decreasing over-expressed ICAM-1.
authors.affiliation: Department of Cardiology, the First Hospital of Jilin University, No 71 XinMin Road, Changchun, Jilin, China.
authors.forename: Bing
authors.initials: B
authors.lastname: Du
authors.forename: Guoliang
authors.initials: G
authors.lastname: Xu
authors.forename: Hongyan
authors.initials: H
authors.lastname: Cao
authors.forename: Wenpeng
authors.initials: W
authors.lastname: Cui
authors.forename: Shumei
authors.initials: S
authors.lastname: Lin
authors.forename: Yunyang
authors.initials: Y
authors.lastname: Liu
authors.forename: Ling
authors.initials: L
authors.lastname: Qin
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000097:blood / Q000188:drug therapy* / Q000235:genetics; D000069059:Atorvastatin; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000187:drug effects*; D006538:Heptanoic Acids / Q000494:pharmacology*; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis / Q000235:genetics*; D008297:Male; D011758:Pyrroles / Q000494:pharmacology*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics*; D011817:Rabbits; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1; D000069059:Atorvastatin