Hydrogen Saturated Saline Lung Injury Protection Of Rats With Severe Acute Pancreatitis And The Experimental Study Of JNK Signaling Pathways Regulating

objective：Exploring Intravenous injection of saturated hydrogen salinesolution Whether protect sodium taurocholate induction of severe acutepancreatitis associated lung injury in rats and to explore its actionmechanism from JNK signaling pathways control.Methods:1. preparationof Hydrogen saturated saline solution: high pressure of hydrogenproduction by hydrogen generator, then high-pressure hydrogen bubbledinto saturated in sodium chloride solution concentration, is now active.2.in severe acute pancreatitis associated lung injury in rats model of theestablishment and processing:54healthy male SD rats were randomlydivided into Sham-operated group (Sham), model group (SAP+NS) andhydrogen water treatment group (SAP+H2), and each subdivided into6h、12h、24h three time points each time point6rats. Sham group rats openclosed abdomen after turning of the pancreas several times, don’t makeother processing, SAP+NS group and SAP+H2group model of severeacute pancreatitis associated lung injury were established by retrogradeinjection of bile pancreatic duct openings(0.1ml/min) with5%sodiumtaurocholate (1ml/kg), the modeling success after1h by tail vein injection,respectively, the same amount of saline or hydrogen saturated saline(5ml/kg). Each group respectively in6h、12h、24h three time points to be put to death in the rat, collect serum、lung tissue and pancreatic tissue.ELISA detect content of TNF-a、IL-1β in the serum；spectrophotometermethod detect the activity of myeloperoxidase (MPO) In the lung tissue；Fluorescence quantitative PCR method detect expression of theTNF-a-mRNA、IL-1β-mRNA in the lung tissue；Western blot methoddetect expression of P-JNK protein in lung tissue；lung wet dry weightratio reflect the degree of lung edema; And HE staining of the pancreas,lung tissue do the pathology examination. The above data collected byusing mean（X—±S）said and dealt with statistical treatmeat Using SPSS17.0statistical software.The comparison of the sample mean use varianceanalysis;besides,the correlation of both use linear correlation andregression analysis, P <0.05, the difference was statistically significant.Results:(1) the SAP+NS group and SAP+H2group contents of TNF-a inthe serum、the level of TNF-a-mRNA expression in lung tissue、P-JNKprotein expression in lung tissue, lung wet dry weight ratio were higherthan Sham group at6h、12h、24h each time point (P <0.05), SAP+H2group compared with SAP+NS group, at all time points SAP+H2groupwere lower than SAP+H2group (TNF-a content：204.1±8.5VS215.3±6.0，P<0.05；122.4±10.3VS263.2±7.4，P<0.05；84.1±8.6VS288.0±5.6，P<0.05.The TNF-a-mRNA expression level:2.81±0.09VS3.94±0.20，P<0.05；2.51±0.11VS4.40±0.24，P<0.05；1.77±0.06VS6.00±0.37，P<0.05.P-JNK protein expression:11.29±0.01VS11.77±0.01，P<0.05；10.59±0.02VS12.73±0.01， P<0.05；9.43±0.01VS14.12±0.01， P<0.05.Lung wet dry weight ratio:3.7±0.2VS4.2±0.2，P<0.05；3.3±0.3VS4.9±0.2，P<0.05；3.2±0.2VS4.6±0.3，P<0.05.)(2) the SAP+NS group andSAP+H2group content of IL-1β in the serum, pancreas and lung tissuepathology score, MPO activity in the lung tissue, IL-1β-mRNA expressionlevel in lung tissue, were higher than Sham group at6h、12h、24h all timepoints (P <0.05), compared with SAP+NS group, change of SAP+H2group is no statistical difference at the time of6h, SAP+H2group werelower than SAP+NS group when the12h、24h (IL-1β content:80.3±8.3VS215.4±10.4，P<0.05；59.3±8.2VS254.3±8.6，P<0.05.Pancreas and lungtissue pathology score:7.5±1.1VS9.5±0.4，P<0.05；7.3±0.4VS9.8±0.3，P<0.05。4.6±0.2VS5.1±0.2，P<0.05；3.8±0.3VS6.3±0.4，P<0.05. MPOactivity:3.3±0.2VS4.7±0.2， P<0.05；3.1±0.1VS4.9±0.2， P<0.05.IL-1β-mRNA expression:1.77±0.16VS1.97±0.11，P<0.05；1.29±0.03VS2.92±0.26，P<0.05.)(3) the Person correlation analysis showed that theP-JNK protein expression in lung correlated with degree of lung tissuedamage. Conclusion:1. The tail vein injection hydrogen saturated salinefor APALI have certain protective treatment.2. Hydrogen saturated salinemay be selective oxidation effect through its inhibiting the activation ofJNK cell signaling pathways to achieve the protection of APALI.