title: [Effects of proliferator-activated receptor-γ agonist on vascular endothelial injuries in septic rats].
abstract: OBJECTIVE
  To explore the effects of rosiglitazone, a synthetic ligand of proliferator-activated receptor-γ (PPAR-γ) on vascular endothelial injuries in septic rats.
  
  
  METHODS
  A total of 40 male Sprague-Dawley rats were randomly divided into 4 groups of vehicle control, lipopolysaccharide (LPS), pretreatment of rosiglitazone (ROSI) and pretreatment of PPAR-γ antagonist 2-chloro-5-nitroaniline (GW9662) (n=10 each). At 4 hours post-intervention, blood samples were collected to detect the expression of PPAR-γ by immunocytochemistry and image analysis. And the following parameters of vascular endothelial injury were measured: Vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), angiopoietin-2 (Ang-2), thrombomodulin (TM), anti-thrombin III (AT-III), tissue factor (TF), von Willebrand factor (vWF) and circulating endothelial cell (CEC).
  
  
  RESULTS
  ① In ROSI group, the expression of PPAR-γ was significantly higher than that in LPS group (P<0.01). In GW9662 group, the expression of PPAR-γ had no significant difference compared to vehicle control group (P>0.05). ② The serum concentrations of VCAM-1, ICAM-1, Ang-2, TM, AT-III, TF and vWF were significantly higher in LPS group than those in vehicle control group (P<0.01). The concentrations of these parameters in ROSI group were significantly lower than those in LPS group (P<0.01). In GW9662 group, the concentrations of these parameters had no significant difference compared with LPS group (P>0.05). ③ The numbers of CEC were significantly higher in LPS group than those in vehicle control group (P<0.01). And the numbers of CEC were significantly lower in ROSI group than those in LPS group (P<0.01). In GW9662 group, the numbers of CEC had no significant difference compared with LPS group (P>0.05).
  
  
  CONCLUSIONS
  Proliferator-activated receptor-γ agonist improves sepsis-induced vascular endothelial injury. And its mechanism may be through stabilizing vascular endothelial cell for improving serious inflammatory reaction and blood coagulation dysfunction.
authors.affiliation: Department of Critical Care Medicine. Yantai Yuhuangding Hospital, Yantai 264000, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Critical Care Medicine. Yantai Yuhuangding Hospital, Yantai 264000, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Dai
authors.affiliation: Department of Critical Care Medicine. Yantai Yuhuangding Hospital, Yantai 264000, China.
authors.forename: Luxin
authors.initials: L
authors.lastname: Yu
authors.affiliation: Department of Critical Care Medicine. Yantai Yuhuangding Hospital, Yantai 264000, China; Email: sunyizhu@126.com.
authors.forename: Yizhu
authors.initials: Y
authors.lastname: Sun
mesh_terms: D042702:Angiopoietin-2; D000813:Anilides; D000818:Animals; D004730:Endothelium, Vascular; D018799:Intercellular Adhesion Molecule-1; D008070:Lipopolysaccharides; D008297:Male; D047495:PPAR gamma; D051381:Rats; D017207:Rats, Sprague-Dawley; D000077154:Rosiglitazone; D018805:Sepsis; D045162:Thiazolidinediones; D013925:Thromboplastin; D019010:Vascular Cell Adhesion Molecule-1
chemical_list: C457499:2-chloro-5-nitrobenzanilide; D042702:Angiopoietin-2; D000813:Anilides; D008070:Lipopolysaccharides; D047495:PPAR gamma; D045162:Thiazolidinediones; D019010:Vascular Cell Adhesion Molecule-1; D000077154:Rosiglitazone; D018799:Intercellular Adhesion Molecule-1; D013925:Thromboplastin