| Objective: Acute lung injury (ALI) is characterized by permeability pulmonary edema as a clinical syndrome.The acute respiratory failure's main pathological basis is pulmonary edema, but its pathogenesis has not yet been fully clarified. The occurrence of pulmonary edema after ALI, although many factors involved.But the main couse is that the removal of lung liquid and exudation are imbalance. The past, people generally believe that pulmonary edema mainly due to pulmonary microvascular endothelial cells (PMEC) was damaged, and had inadequate understanding of the role about aquaporins (AQPS) which existence on lung tissue under pathophysiological. AQP-1 mainly role is conveying the pulmonary interstitial fluid .So,it can relieve the degree of pulmonary edema. Ulinastatin (UTI) is able to inhibit trypsin, phospholipase A2, hyaluronidase, elastase, etc. On the lysosome membrane,it has a stabilizing effect, and has the effect of inhibiting the release of inflammatory mediators, and has the effect of the removal of excessive oxygen free radicals and other functions. Our animal experiments confirmed that ulinastatin has an effective role in treatment of acute lung injury, reducing pulmonary edema, but its mechanism of alleviate pulmonary edema is not very clear. For this perpers, in this experiment we copyed oleic acid-induced acute lung injury model, and used ulinastatin to treat acute lung injury, to study the changes of expression about AQP-1 on acute lung injury ,and their the explore possible mechanisms of ulinastatin on acute lung injury, in order to provide a theoretical basis for ulinastatin in the treatment of acute lung injury.Methods: The animal modle of acute lung injury was established by injecting oleic acid into the external jugular vein of rat.Forty healthy wistar rat of masculinity weighting 250g were randomly divided into four groups: control group (10), model group (10), ulinastatin group (10), treatment group (10), four hours later, each group animals were separately collected and drawn blood in the external carotid artery for arterial blood gas analysis ,IL-6, TNF-αcontent in serum was examined by radioimmunoassay, detect expression of AQP-1 was detected by immunohistochemical,Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detected the expression of AQP-1mRNA. Results: 1 the general performance of thr animals: The animals were anesthetized by 10% urethane , The ALI model ware esterblished by injecting 0.1ml/kg oleic acid into rats external jugular vein.The rats showed shortness of breath, lips cyanosis, difficulty in breathing, nodded breathing, and wheezing sound,the respiratory frequency was 80-100 times before delivery to 120-150 times, the situation of the treatment group has improved after ulinastatin was gived, but the control group and ulinastatin group did not change significantly.2 the results of blood gas analysis: In the model group, oxygen saturation and blood oxygen partial pressure was lower than the that in control group (p <0.05), oxygen saturation and blood oxygen partial pressure of ulinastatin group compare with the control group's were no significant difference (p> 0.01) the treatment group oxygen saturation and blood oxygen partial pressure is higher than the model group (p <0.05)3 Radioimmunoassay results: The model group, IL-6 and TNF-αlevels in serum is higher than those in the control group (p <0.05), IL-6 and TNF-αlevels in serum of ulinastatin group had no significant difference with those results in the control group(p> 0.01).In the treatment group, IL-6 and TNF-αcontent in serum is lower than the model group (p <0.05)4 Immunohistochemistry results: The model group,expression of AQP-1 is less than those in the control group (p <0.05), AQP-1 expression level was no significant difference between the Ulinastatin group and the control group(p> 0.01), treatment group, the expression of AQP-1 was higher than the model group in the expression levels (p <0.05)5 RT-PCR results: the model group in the expression of AQP-1mRNA is lower than those in the control group in expression (p <0.05), ulinastatin group the amount of AQP-1mRNA with the control group was no difference in the expression levels (p > 0.01),treatment group the expression of AQP-1mRNA model group was higher than expression in the control group (p <0.05)Conclusion: The expression levels of AQP-1mRNA and AQP-1 in ALI model group decreased significantly than that in the control group, AQP-1 expression reduction may be the cause of pulmonary edema in acute lung injury. In the treatment group, AQP-1 expression also increased significantly, but ulinastatin had no effect about aquaporin-1.So we speculated that ulinastatin may be by reducing IL-6, TNF-αand other inflammatory mediators in order to regulate the expression of AQP-1, to lighten pulmonary edema in acute lung injury. |
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