Effect Of Dexamethasone On The Variation Of HMGB1,IL-18 And CNIC In Severe Acute Pancreatitis-induced Hepatic Injury

Objective:To investigate pathological changes,variation of IL-18,CINC in serum and HMGB1 levels in liver and to explore the therapeutic effect of dexamethasone in severe acute pancreatitis -associated hepatic injury model in rats.Methods:Male SD rats were divided into three groups randomly:the control group, the experimental group and the intervention group.In the control group,laparotomy were performed,duodenum and pancreas were flipped only.In the experimental group,acute necrotizing pancreatitis model was induced in rats by retrograde injection of 5%sodium taurocholate into biliopancreatic duct.In the intervention group,dexamethaso -ne(5mg/kg) was injected into rump musle of rats after models were developed.At 6,12 and 24 hours after model were developed,IL-18,CINC in serum were quantitated using ELISA kits. HMGB 1 levels in liver and serum were detected by Western blotThe severity of pancreatitis and liver injury was determined by local pathological lesion(gross and histopathologic scoring).The effect of dexamethasone were observed at the same time.Results:1.In the experimental group,the pathological score increased at 6 hours after SAP model induction,and more at 12 and 24 hours(P＜0.05);higher than the control group(P＜0.05);In the intervention group,the pathological score was lower than in the experimental group(P＜0.05)2.In the experimental group,the IL-18 in serum increased at 6 hours after SAP model induction,and more at 12 and 24 hours(P＜0.05);higher than the control group(P＜0.05);In the intervention group,IL-18 was lower than in the experimental group(P＜ 0.05)3.In the experimental group,the CINC in serum increased at 6 hours after SAP model induction,reached the peak 12h later and decrease in 24 hours(P＜0.05);higher than the control group(P＜0.05);In the intervention group,CINC was lower than in the experimental group(P＜0.05)4.In the experimental group,the HMGB 1 in serum and liver increased at 6 hours after SAP model induction,and more at 12 and 24 hours(P＜0.05),higher than the control group(P＜0.05).In the intervention group,HMGB1 in serum and liver was lower than in the experimental group(P＜0.05)Conclusions:1.IL- 18 perhaps involved in the development of acute pancreatitis-associated hepatic injury.It make the hepatic injury progressive increase.Treatment with Dexame -thasone may reduce IL-18 levels in serum.2.CINC perhaps involved in the development of acute pancreatitis-associated hepatic injury.The function of CINC is less than IL-18 in severe acute pancreatitis -associated hepatic injury.Treatment with Dexamethasone may reduce CINC levels in serum.3.HMGB1 in serum and liver perhaps involved in the development of acute pancreatitis-associated hepatic injury.The level of HMGB1 in serum was lower than in liver,explain it maybe originate from liver.HMGB1 can be looks as the standard of diagnosis of acute pancreatitis- associated hepatic injury.Treatment with Dexamethasone may reduce HMGB1 levels in serum and liver.