Rosiglitazone attenuates the severity of sodium taurocholate-induced acute pancreatitis and pancreatitis-associated lung injury.
OBJECTIVE
In addition to the effect of regulating adipocyte differentiation and insulin sensitivity, peroxisome proliferator activated receptor-gamma (PPAR-gamma) ligands also exhibit anti-inflammatory effect. However, the mechanisms concerning how PPAR-gamma ligands affect acute pancreatitis and pancreatitis-associated lung injury have not been fully elucidated. This study investigated the effect of rosiglitazone, a PPAR-gamma ligand, on acute pancreatitis and pancreatitis-associated lung injury in the rat pancreatitis model induced by sodium taurocholate.


METHODS
Acute pancreatitis was induced by retrograde infusion of 5% sodium taurocholate (1 mL/kg) into the bile-pancreatic duct. Rosiglitazone (6 mg/kg) was administered via the femoral vein 30 min prior to the infusion of sodium taurocholate. The severity of pancreatitis was evaluated by serum amylase level, myeloperoxidase activity, and pathology. Pancreatitis-associated lung injury was evaluated by myeloperoxidase activity, the magnitude of pulmonary edema and pathology. Intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha mRNA expression were studied using reverse transcriptase polymerase chain reaction. ICAM-1 protein expression was studied using Western blot analysis.


RESULTS
Prophylactic administration of rosiglitazone attenuated (1) serum amylase level; (2) myeloperoxidase activity of pancreatic and pulmonary tissue; (3) expression of tumor necrosis factor-alpha and ICAM-1 in pancreas and lung; (4) pancreas and lung pathological damage.


CONCLUSIONS
Our study demonstrated that rosiglitazone exerts a protective effect against sodium taurocholate-induced pancreatic and pulmonary injury.
Chen
Chen
C
Department of General Surgery, Renmin Hospital of Wuhan University, PR China.
Xu
Sheng
S
Wang
Wei-Xing
WX
Ding
You-Ming
YM
Yu
Kai-Huan
KH
Wang
Bin
B
Chen
Xiao-Yan
XY
D000681:Amylases / Q000097:blood; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D004195:Disease Models, Animal; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D055370:Lung Injury / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D047495:PPAR gamma / Q000378:metabolism; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000150:complications / Q000517:prevention & control*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D000077154:Rosiglitazone; D013656:Taurocholic Acid / Q000627:therapeutic use*; D045162:Thiazolidinediones / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000894:Anti-Inflammatory Agents, Non-Steroidal; D007004:Hypoglycemic Agents; D047495:PPAR gamma; D045162:Thiazolidinediones; D014409:Tumor Necrosis Factor-alpha; D000077154:Rosiglitazone; D018799:Intercellular Adhesion Molecule-1; D013656:Taurocholic Acid; D009195:Peroxidase; D000681:Amylases