Effect of peroxisome proliferator-activated receptor-γ ligand on acute necrotizing pancreatitis associated lung injury in rats

Objective To investigate the effect of Rosiglitazone on acute necrotizing pancreatitis (ANP) associated lung injury in rats and its potential mechanism. Methods Fifty-four male Wistar rats were randomly divided into sham operation group (SO group), ANP group and Rosiglitazone pretreatment group (Rosi group). ANP model was induced by retrograde infusion of 5% sodium taurocholate into the biliopancreatic duct. The rats of SO group, ANP group were injected with 10% dimethyl sulfoxide (DMSO) (0.2 ml/100 g) via femoral vein 30 minutes prior to the operation. In Resi group Rosiglitazone partes aequales (6 mg/kg), which was dissolved in 10% DMSO, was injected. Rats were killed at 3 h, 6 h and 12 h after induction. The serum amylase, lung myeloperoxidase (MPO), lung wet/dry (W/D) weight ratio, protein content of bronchoalveolar lavage fluids (BALF) were measured, and pancreas and lung pathologic changes were evaluated. RT-PCR was used for detecting the levels of TNF-α and ICAM-1 mRNA in lung tissue. Results In ANP group, the values a of serum amylase, MPO, W/D weight ratio, protein content of BALF, pancreas and lung pathologic score, lung TNF-α and ICAM-1mRNA expression increased corresponding to the duration of ANP course, and the corresponding values at 12 h were (5353.0±728.2) U/L, (1.12±0.14) U/g, 3.00±0.14, 0. 438±0.056, 11.17±0.93 and 8.17±0.75, respectively, which were significantly higher than those in the SO group (P<0. 05 or P<0.01). The corresponding values in the Rosi group were (2847.4±841) U/L, (0.84±0.06) U/g, 2.13±0.36, 0.283±0.078 g/L, 7.75±0.27, 4.33±0.82, 0.26±0.04 and 0.84 ±0.02, respectively, which were significantly higher than those in the SO group (P <0. 05 or P <0.01). Conclusions Rosiglitazone had protective effect on lung injuries in ANP rats through down-regnlating the expression of TNF-α and ICAM-1 mRNA. Key words: Pancreatitis, acute necrotizing;  Peroxisome proliferator-activated receptors;  Tumor necrosis factor-α;  Lung injury;  Intercellular adhesion molecule-1