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Objective To investigate the animal model of acute lung injury (ALI) induced by caudal vein injection of trypsin in rats and to evaluate the model.Methods The model of lung injury was established by caudal vein injection of trypsin in rats.The rats were killed at the time point of 3 h,6 h,12 h,24 h,and 24 h and then the pathological changes of structure of lungs,peripheral blood neutrophil count,arterial blood gas analysis and lung wet/dry (W/D) weight ratio in rats were measured and observed.Results The results of hematoxylin eosin (HE) staining showed that there was no obvious pathological changes in lung tissues of the control group,while alveolar and pulmonary septal edema,thickening,and a large number of inflammatory cells infiltration in the lung tissues of the model group.Compared to the control group,the peripheral blood neutrophil counts,W/D and PaCO2 were significantly increased,PaO2 was significantly decreased (P ＜0.01).There was significant differences in the number of peripheral blood neutrophils,PaCO2,W/D and PaO2 between the model groups (P ＜ 0.01).Conclusions The rat model of ALI induced by trypsin can successfully simulate the lung damage caused by the release of a large number of trypsin when severe acute pancreatitis occurred.
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Objective To investigate the role of p38 MAPK in the trypsin-induced injury in human esophageal epithelial cells.Methods Primary cultured human esophageal epithelial cells were stimulated with trypsin (20,40,and 80 μg/ml) for4 hours,phosphorylation of p38 MAPK was evaluated by Western blotting.Primary cultured human esophageal epithelial cells were stimulated with trypsin (40 μg/ml) and treated with p38 MAPK inhibitor (SB203580,1 and 10 μmol/L) simultaneously.Four hours later,the cells were collected for analysis.Results Western blotting results revealed that stimulation with trypsin enhanced phosphorylation of p38 MAPK,indicating that trypsin activated p38 MAPK in esophageal epithelial cells.SB203580 treatment suppressed trypsin-induced expression of pro-inflammatory cytokines including interleukin-8 (IL-8),cyclooxygenase 2 (COX2),and tumor necrosis factor alpha (TNFcα).Finally,SB203580 treatment suppressed trypsin-induced upregulation of protein expression of inducible nitric oxide synthase (iNOS),and subsequently reduced nitric oxide (NO) levels.Conclusions The regulation of p38 MAPK was involved in the trypsin-induced injury in esophageal epithelial cells.