ObjectiveTo investigate the possible protective effect of zerumbone on pancreatic injury in severe acute pancreatitis (SAP) rats, and to provide a theoretical basis for prevention and treatmen of severe acute pancreatitis. MethodsSeventy male Wistar rats were randomly divided into four groups:normal control group (NC group, n=10), SAP group (n=40), Zerumbone pretreatment group (ZER group, n=10), and Zerumbone drug control group (ZER-CON group, n=10). Rats of SAP group were divided into four time points of 1 h, 3 h, 6 h, and 12 h (n=10 each time point). SAP models were induced by retrograde injection of 5% sodium taurocholate (0.1 mL/100 g) in biliopancreatic duct in SAP group and ZER group. Rats were injected isotonic saline solution instead of taurocholate as a control in NC group and ZER-CON group. Zerumbone solution (10 mg/kg) was administered via femoral vein half an hour prior to establishing models in ZER group and ZER-CON group. All rats except SAP group were sacrificed at 12 h time point after the induction of SAP. The rats in SAP group were sacrificed at 1 h, 1 h, 3 h, 6 h and 12 h time point after induction of SAP. The mortality, ascites, serum amylase (AMY), phospholipase, and pathological examination of pancreas were observated or detected. The expression of nuclear factor-kappa B (NF-κB) p65 in pancreatic tissues was evaluated by immunohistochemistry assay. ResultsThere were no difference of the levels of mortality, ascites, serum AMY, phospholipase, pathological examination, and NF-κB p65 location expression of pancreas between the ZER-CON group and NC group (P>0.05). The above indexes in SAP group were significantly higher than those in NC group (P<0.05). However, those in ZER group were significantly lower than in SAP group (P<0.05), and higher than in NC group (P<0.05). ConclusionsZerumbone can reduce the mortality and ascites, effectively alleviate the enzyme, pathological injury, and NF-κB p65 location expression in pancreatic tissue following SAP. It may indicate that zerumbone can protect pancreatic injury in SAP via NF-κB pathway.
ObjectiveTo investigate The role of tumor necrosis factor-α (TNF-α) in pancreatitis-associated adrenal cells' apoptosis of severe acute pancreatitis (SAP). MethodsForty Wistar rats were randomly divided into sham operation group (SO group) and SAP group by random number method, the SAP group was divided into 3, 6, 12, and 24 h 4 subgroups, 8 rats in each group. SAP model was induced by retrograde injection of 5% sodium taurocholate into the bilipancreatic duct. At 3, 6, 12, and 24 h after operation, serum amylase and lipase was measured, adrenal injury was evaluated by histological examination, apoptosis of the adrenal cells was observed by TUNEL method, and expressions of TNF-α and Caspase-3 protein were detected by Western blot. ResultsThe levels of serum AMY and LIP, histopathological scores of pancreatic tissues and adrenal tissues at each time point after operation in SAP group increased significantly than SO group (P < 0.05). With the duration extension of SAP, the apoptosis index of adrenal cells in SAP group progressively heightened, and were higher than those in the SO group (P < 0.05). And the expressions of TNF-α and Caspase-3 protein in adrenal tissues of SAP group gradually increased, at 24 h this data slightly decreased, but still higher than SO group (P < 0.05). ConclusionTNF-α may be involved in the pathogenesis of adrenal injury in SAP rats by activate the protein expression of Caspase-3.