| Objective: Peroxisome proliferator-activated receptor-γ(PPARγ) are members of the nuclear receptor superfamily containing transcription factors regulating gene expression. PPARγhave attracted attention so far as key factors in lipid metabolism, insulin sensitivity, and apoptosis. Recently, growing evidence points to their implication in the regulation of the immune response, particularly in inflammation control. This study was designed to determine the protective effects and the molecular mechanisms of rosiglitazone, a specific potent PPARγagonist, on the development of severe acute pancreatitis (SAP), associated liver injury and hyperglycaemia in rats.Methods: Male Sprague-Dawley (SD) rats (280±20g) were randomly allocated into three groups (n=24 for each group). Sham group: sham-operated animals served as control, operation was executed and sodium taurocholate was not injected. SAP group: SAP was induced in male SD rats by the retrograde injection of 5% sodium taurocholate (1ml/kg) into the biliopancreatic duct. Rosiglitazone group: same as SAP group, but 1% rosiglitazone (1ml/kg) was administered intraperitoneally an hour before operation. Rats were killed by abdominal aorta exsanguination at 3, 6 and 12h after induction of acute pancreatitis. Serum activity of amylase, glucose and ALT level were measured. The pancreatic tissue was divided into four parts: I, Paraffin section, hematoxylin and eosin stain, histologic score was performed. II, Pancreatic water content was performed. III, Pancreatic MPO, iNOS, NO level were measured. IV, The mRNA of PPARγand iNOS level were measured by semiquantitative RT-PCR. The liver tissue was divided into three parts: I, Paraffin section, hematoxylin and eosin stain, histologic score was performed. The expression of NF-κB was evaluated by immunohistochemical method. II, Hepatic MPO,... |
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