Peroxisome proliferator-activated receptor ? agonist attenuates ICAM-1 and CINC-1 expression in lungs of rats with acute lung injury
- VernacularTitle:PPAR?受体激动剂抑制急性肺损伤大鼠肺脏粘附分子和趋化因子的表达
- Author:
Dong LIU
;
Bangxiong ZENG
;
Shihai ZHANG
;
Zhilong GENG
;
Shifan ZHANG
- Publication Type:Journal Article
- Keywords:
Peroxisome proliferator-activated receptor ?;
Lung injury,acute;
Lipopolysaccharides;
Intercellular adhesion molecule-1;
Chemokines;
Rosiglitazone
- From:
Chinese Journal of Pathophysiology
2000;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the effects of rosiglitazone(ROSI),an agonist of peroxisome proliferator-activated receptor ?(PPAR?),on the lung expression of intercellular adhesion molecule-1(ICAM-1) and cytokine-induced neutrophil chemoattractant(CINC) in rats with acute lung injury. METHODS: Thirty-six male Wistar rats were randomly divided into six groups: control group,ROSI group,GW9662(a PPAR? antagonist) group,lipopolysaccharide(LPS,6 mg/kg,iv) group,ROSI-LPS group(0.3 mg/kg ROSI iv 30 min prior to LPS) and GW9662-ROSI-LPS group(0.3 mg/kg GW9662,iv,20 min before ROSI).Four hours after LPS injection,wet/dry weight(W/D) ratio,myeloperoxidase (MPO) activity,malondialdehyde(MDA) and CINC-1 concentrations were assayed in the lung tissues.Immunohistochemical analysis of ICAM-1 expression was also studied.RESULTS: Pretreatment with ROSI significantly attenuated LPS-induced increases in W/D ratio,MPO activity,MDA and CINC-1 concentrations as well as ICAM-1 expression in the lung tissues.The specific PPAR? antagonist GW9662 antagonized the effects of ROSI.CONCLUSION: Pretreatment with ROSI reduces LPS-induced lung injury in rats.The mechanism involves inhibition of the lung expression of ICAM-1 and CINC-1 by the activation of PPAR?.
