Rosiglitazone, an agonist of peroxisome proliferator-activated receptor γ, reduces pulmonary inflammatory response in a rat model of endotoxemia

摘要: Objective: The effect of rosiglitazone, a potent peroxisome proliferator-activated receptor γ (PPAR-γ) agonist, on pulmonary inflammation in endotoxemia was investigated. Materials and methods: Male Wistar rats were given either lipopolysaccharide (LPS, 6 mg/kg i.v.) or saline, pretreated with rosiglitazone (0.3 mg/kg its vehicle (dimethyl sulphoxide) 30 min before LPS. selective PPAR-γ antagonist GW9662 20 min rosiglitazone. Wet/dry weight (W/D) ratio, myeloperoxidase (MPO) activity, malondialdehyde (MDA) as well TNF-α CINC-1 concentrations measured lung tissues 4 h after LPS injection. Expression ICAM-1, NF-κB p65 also determined by immunohistochemistry Western blot analysis. Results: Rosiglitazone pretreatment significantly attenuated the increases W/D MPO activity MDA levels, reduced overproduction expression ICAM-1 following endotoxemia. inhibited nuclear localization up-regulated protein. specific abolished Conclusion: These findings suggest that agonists might be used therapeutic agents therapy inflammatory injury related to