Effect of PEP-1-SOD1 on Cell Apoptosis in SAP Rats / 胃肠病学

ABSTRACT

Background: Severe acute pancreatitis (SAP) is characterized by diffuse pancreatic hemorrhage and tissue necrosis with high mortality. PEP-1-SOD1 is a fusion protein synthesized by genetic engineering technology. It has a high stability and certain anti-inflammatory effects. Aims: To investigate the effect of PEP-1-SOD1 on cell apoptosis in SAP rats. Methods: A total of 24 male Wistar rats were divided into control group, SAP group and experimental group. SAP rat model was established by infusion of 5% sodium taurocholate. Thirty minutes before the establishment, rats in experimental group were abdominal subcutaneously injected with 8.0 mg/kg PEP-1-SOD1, and rats in SAP group were injected with same dose of 0.9% NaCl solution. Histopathological score of pancreatic tissue were evaluated; apoptosis of pancreatic acinar cell was determined by TUNEL. The mRNA and protein expressions of caspase-3 were detected by fluorescent quantitative PCR and Western blotting, respectively. Results: After 24 hours of model establishment, serum amylase and lipase, mRNA and protein expressions of caspase-3 in SAP group and experimental group were significantly higher than those in the control group (P<0.05), however, serum amylase and lipase in experimental group were significantly lower than those in SAP group (P<0.05), while mRNA and protein expressions of caspase-3 were significantly increased (P<0.05). After 6, 24 hours of model establishment, histopathological score, apoptotic index in SAP group and experimental group were significantly higher than those in the control group (P<0.05), however, histopathological score in experimental group was significantly lower than that in SAP group (P<0.05), while apoptotic index was significantly increased (P<0.05). Conclusions: PEP-1-SOD1 may increase the apoptosis of pancreatic acinar cells through regulating the expression of apoptosis related gene caspase-3 in SAP rats, thereby reducing the pathological damage of pancreatic tissue and promoting the recovery of pancreatic function.