title: Urinary Trypsin Inhibitor Reduced Inflammation Response Induced by Hyperlipidemia.
abstract: OBJECTIVE
  Atherosclerosis is recognized as a chronic inflammatory disease. The aim of this study was to examine the role of urinary trypsin inhibitor (UTI) in inflammation response induced by hyperlipidemia in rabbits.
  
  
  METHODS
  Thirty rabbits after injury of the right iliac artery endothelium were randomly divided into 3 groups: control group, model group, and UTI group. Iliac arteries were isolated and histology was performed on arterial regions that were injured by balloon after 8 weeks. Neointimal thickness (NT) and neointimal to media radio (N/M) were measured. Blood lipids, interleukin 6, and tumor necrosis factor-α were evaluated. Macrophages were evaluated by immunohistochemical analysis. MicroRNA-181b (miR-181b) was measured by reverse transcriptase-polymerase chain reaction.
  
  
  RESULTS
  Urinary trypsin inhibitor therapy decreased serum inflammatory factor levels without significant changes in blood lipids. Compared with model group, UTI reduced macrophage infiltration of iliac artery (13.91 ± 2.03% vs 24.21 ± 8.94%, P < .01). Hyperlipidemia reduced the expression of miR-181b and increased NT and N/M ratio. Systemic administration of UTI rescued miR-181b expression and inhibited neointimal formation.
  
  
  CONCLUSIONS
  Urinary trypsin inhibitor could reduce neointimal hyperplasia by inhibiting inflammatory response induced by hyperlipidemia and may become a potential antiatherosclerosis supplement.
authors.affiliation: Department of Emergency, Second Affiliated Hospital of Harbin Medical University, Harbin, Hei Long Jiang, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Deng
authors.affiliation: Department of Emergency, Second Affiliated Hospital of Harbin Medical University, Harbin, Hei Long Jiang, China kjygtg123@163.com.
authors.forename: Junying
authors.initials: J
authors.lastname: Kong
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D050197:Atherosclerosis / Q000188:drug therapy / Q000473:pathology; D004730:Endothelium, Vascular / Q000473:pathology; D006023:Glycoproteins / Q000494:pharmacology*; D006949:Hyperlipidemias / Q000188:drug therapy* / Q000473:pathology*; D007083:Iliac Artery / Q000293:injuries; D015850:Interleukin-6 / Q000096:biosynthesis; D008055:Lipids / Q000097:blood; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D008297:Male; D035683:MicroRNAs / Q000378:metabolism; D058426:Neointima / Q000473:pathology; D011817:Rabbits; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D006023:Glycoproteins; D015850:Interleukin-6; D008055:Lipids; D035683:MicroRNAs; D014409:Tumor Necrosis Factor-alpha; C028665:urinastatin
keywords: atherosclerosis; hyperlipidemia; inflammation