RÉSUMÉ
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.
RÉSUMÉ
Objective To investigate the neuropretective effect of PEP-1-SOD1 pretreatment on the parietal cortex of mice with cerebral infarction. Methods Healthy Kunming-mice were assigned randomly into sham-operated group, model group and PEP-1-SOD1 precondition group (n=15). And the models of permanent middle cerebral artery occlusion (pMCAO) were established in the later 2 groups.The mice in the sham-operated group and model group were intraperitoneally injected with 200-ul saline and the mice in the PEP-1-SOD1 precondition group were intraperitoneally injected with 200-ug PEP-1-SOD1 fusion protein 30 min before the model inducement, respectively. The parietal cortex was dissected 24 h after the success of model making. Triphenyltetrazolium chloride (TTC) staining was employed to detect the volume of infarction and TUNEL staining was used to detect the cell apoptosis;the content of malondialdehyde (MDA) was measured using the thiobarbituric acid (TBA) method and the activity of SOD 1 was measured by xanthine oxidase method. Results The volume of infarction in the PEP-1-SOD1 precondition group was obviously smaller than that in the model group (P＜0.05).Compared with those in the model group, significantly reduced apoptotic neural cells were noted in the PEP-1-SOD1 precondition group (P＜0.05). Compared with model group, increased activity of SOD1 and decreased level of MDA were found in the cell apoptosis (P＜0.05). Conclusion Precondition with PEP-1-SOD1 fusion protein can efficiently protect the parietal cortex of mice with cerebral infarction.