P38MAPK Signal Pathway Inhibitor SB203580’s Role Of Regulation Of TNF-α Expression In The Pancreatic Tissue Of Rats With Severe Acute Pancreatitis

Background:Severe acute pancreatitis is one of the most difficult disease, it has high morbidity、bad prognosis and high mortality, and now its mortality is very high..The pathogenesis of serve acute pancreatitis has not yet been fully determined.It has been recognized that the interaction of various cytokines in the signal transduction pathway produce a large variety of inflammatory factors in the pathogenesis of SAP, and thus leed to systemic inflammatory response syndrome(SIRS), eventually leading to multiple organ dysfunction syndrome (MODS).It has been confirmed that P38mitogen activated protein kinase (MAPK) pathway are closely related with the appearance and regulation of various cytokines. so this study create severe acute pancreatitis model in rats to discuss the pathway,and observe the effect of P38MAPK inhibitor SB203580on SAP rats model.Methods:This experimental create the model of serve acute pancreatitis in rats by injection sodium taurocholate to pancreatic duct, and use SB203580to inhibit P38MAPK pathway.We observe the influence of P38MAPK inhibitor SB203580in SAP rats and investigate the effect of P38MAPK on SAP pathogenesis by check the content of amylase and interleukin1β in serum.Results:The expression of TNF-a in SAP group was higher than control group significantly. The express of IL-1β in pancreatic tissue rises with the progress of pancreatitis disease, the expression in SAP group and inhibitor group is higher than that in control group, but the expression in inhibitor group is lower than that in SAP group at all time points(P<0.05).Conclusion:P38MAPK may be involved in the process of severe acute pancreatitis in rats, and SB203580can reduce the release of inflammatory mediators, mitigate the pathological damage in severe acute pancreatitis by prevent the activation of P38MAPK pathway.