title: [Analysis of inflammatory reaction of atherosclerosis model].
abstract: OBJECTIVE
  To analysis and evaluate the inflammatory reaction of atherosclerosis model in rabbits.
  
  
  METHODS
  A model of atherosclerosis in rabbits was estabalished by injury with balloon and high cholesterol diet to observe the dynamic change of serum inflammation markers c-reactive protein, interleukin-1beta and tumor necrosis factor-a, and the relationship between severity of AS lesion and those change.
  
  
  RESULTS
  (1) The levels of TNF-alpha at 4 time points: 1, 6, 10 weeks and 10 weeks + 1 day after balloon injury increased 1.6-fold, 2.2-fold, 4-fold, 2-fold over concurrent control, respectively (P < 0.05, P < 0.01, P < 0.01, P < 0.01), but no significant changes occurred during the observation. (2) At the end of the 6, 10 weeks and 10 weeks + 1 day, the levels of CRP were increased 3.5-fold, 3.6-fold, 3.0-fold than concurrent control (P < 0.01, P < 0.01, P < 0.01), respectively. The levels were increased 2.4-fold at the end of the 6 weeks and 4.1-fold at the end of the 10 weeks and reached the peak compared with the point of 1 week. (3) TNF-alpha and CRP showed a significant positive correlation with the MIT (correlation coefficients were found to be 0.61, 0.64, P < 0.01). (4) At the end of the 1, 6, 10 weeks, the model was provided with general pathological characteristics and the inflammatory reaction of earlier inflammatory reaction phase, fatty streak plaques phase, fibrous plaque phase respectively.
  
  
  CONCLUSIONS
  The model was provided with early and medial phase typical feature of atherosclerotic lesion, and showed a significant positive correlation with the inflammatory factor expression. At the end of the 6 weeks, the formation of fatty streak plaques and obvious inflammatory reaction could be satisfied for the interference in forming process of AS from dimension of inflammatory and screening assays of drugs.
authors.affiliation: Institute of Chinese Materia Medica, China Academy of Chinese Medical Science, Beijing 100700, China.
authors.forename: Yu-Jie
authors.initials: YJ
authors.lastname: Li
authors.forename: Qing
authors.initials: Q
authors.lastname: Yang
authors.forename: Xiao-Gang
authors.initials: XG
authors.lastname: Wen
authors.forename: Xiao-Xing
authors.initials: XX
authors.lastname: Zhu
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000097:blood* / Q000473:pathology; D002097:C-Reactive Protein / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000473:pathology; D005260:Female; D005263:Femoral Artery / Q000473:pathology; D007249:Inflammation / Q000097:blood / Q000473:pathology; D018836:Inflammation Mediators / Q000097:blood*; D053583:Interleukin-1beta / Q000097:blood*; D008297:Male; D011817:Rabbits; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D018836:Inflammation Mediators; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein