The Role of MAPK Signal Transduction in Rats with Experimental Severe Acute Pancreatitis
Xudan Chen
Abstract
Xudan Chen
Abstract
Objective To investigate the role of the p38MAPK signaling pathway in severe acute pancreatitis (SAP) and its specific inhibitor SB203580 on the protective effect of the pancreas. Methods Forty-eight SD rats were randomly divided into control group (C), severe acute pancreatitis (P) and SB203580 group (T). For each group, it was further divided into 2 h and 6 h subgroup, respectively. All the rats were anesthetized with an intraperitoneal injection of 25% urethane (1.5 g/kg). SAP models were induced by injection of 50 g/L sodium taurocholate (4 mL/kg) under the pancreatic membrane. In the normal control group, the rats received isovolumetric injection of 9 g/L normal saline solution. Preoperative treatment group was given orally SB203580 (10 mg/kg) in the T group. The blood samples of the rats in each group were obtained via superior mesenteric vein measuring levels of TNF-α. Results Pancreatic pathological scores were higher in P group than in C group throughout the experimental course (P 0.01). Histopathologic scores in T group were lower than that of P group at 2 h and 6 h. Levels of serum TNF-α in P group were significantly higher than those of C group, respectively (P 0.01) . Levels of serum TNF-α were significantly decreased significantly in T group than those of P group at 2 h and 6 h (P 0.01). At each time point, p38MAPK expression of pancreas in P group was significantly higher than group C and significantly decreased in T group than that in P group. Conclusion p38MAPK signal transduction pathway plays an important role in the development of SAP and its specific inhibitor SB203580 has the protective effect on the pancreas.
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Objective To investigate the role of the p38MAPK signaling pathway in severe acute pancreatitis (SAP) and its specific inhibitor SB203580 on the protective effect of the pancreas. Methods Forty-eight SD rats were randomly divided into control group (C), severe acute pancreatitis (P) and SB203580 group (T). For each group, it was further divided into 2 h and 6 h subgroup, respectively. All the rats were anesthetized with an intraperitoneal injection of 25% urethane (1.5 g/kg). SAP models were induced by injection of 50 g/L sodium taurocholate (4 mL/kg) under the pancreatic membrane. In the normal control group, the rats received isovolumetric injection of 9 g/L normal saline solution. Preoperative treatment group was given orally SB203580 (10 mg/kg) in the T group. The blood samples of the rats in each group were obtained via superior mesenteric vein measuring levels of TNF-α. Results Pancreatic pathological scores were higher in P group than in C group throughout the experimental course (P 0.01). Histopathologic scores in T group were lower than that of P group at 2 h and 6 h. Levels of serum TNF-α in P group were significantly higher than those of C group, respectively (P 0.01) . Levels of serum TNF-α were significantly decreased significantly in T group than those of P group at 2 h and 6 h (P 0.01). At each time point, p38MAPK expression of pancreas in P group was significantly higher than group C and significantly decreased in T group than that in P group. Conclusion p38MAPK signal transduction pathway plays an important role in the development of SAP and its specific inhibitor SB203580 has the protective effect on the pancreas.
Key concepts: Medicine, Acute pancreatitis, Saline, Pancreatitis, Internal medicine, Intraperitoneal injection, Pancreas, Group A