Dynamic Changes of Soluble Fas and IL-2/IL-10 in serum and Fas Expression in Lung in the Rats of Acute Necrotizing Pancreatitis.

Abstract

BackgroundTo investigate the dynamic changes of serum IL-2, IL-10, sFas and IL-2/IL-10 in a rat model with acute necrotizing pancreatitis (ANP). To explore the role of Th1/Th2 polarization and the Fas expression in the lung of rats with ANP.MethodsA total of 64 Sprague-Dawley rats were randomly divided into normal control group and ANP model group. ANP models were induced by injection of 50 g/L sodium taurocholate (4 mL/kg) under the pancreatic membrane. In the normal control group, the rats received isovolumetric injection of 9 g/L normal saline solution. The blood samples in each group were obtained via superior mesenteric vein for measuring IL-2, IL-10 and soluble Fas. The levels of IL-2, IL-10 and soluble Fas were determined by ELISA. The severity of lung injury was evaluated by pathologic score. The expression of Fas in lung was measured by immunohistochemistry.ResultsIn the ANP model group, levels of serum IL-2 were significantly higher than those of control group (P < 0.01), and peaked at 6 hours; levels of serum IL-10 were significantly higher than those of control group at 6 and 12 hours (P < 0.01); the ratios of IL-2/IL-10 were significantly higher than those of control group at 0.5 hours and 2 hours, however, they were significantly lower than those of control group at 6 hours, (P < 0.01), and returned to the normal level (P > 0.05). In Fas/APO-1 assay, there was no significant difference between the two groups. The pathological changes were aggravated significantly in model group compared with the control group. Immunohistochemistry stain showed Fas expression was absent in normal pulmonary tissue, whereas in pulmonary tissue Fas expression gradually increased 0.5 hours after induction of pancreatitis, and reached their peaks at 12 hours.ConclusionsFas are involved in the pathogenesis of pancreatitis associated lung injury, the mechanism might be related to the Fas mediated T helper cell apoptosis.