| Objective To investigate the protective effects of epidermalgrowth factor (EOF) in rats with acute pancreatitis (AP), some assays were performed like: Ascites volume, amylase activity in serum, pancreatic histology, and apoptosis index (AI), Malondialdehyde (MDA) of jejunum and pancreas.Methods Seventy-two male Sprague-Dawley rats were anesthetized with sodium pentobarbital (35mg.kg-1, intraperioneally). AP wasinduced by intraductal infusion of 35g.L-1 sodium taurocholate solution (1.0 mL.kg-1) after clamping the proximal end of the common bile duct and puncture the biliary-pancreatic duct. Then the rats were randomly divided into 3 groups: Control group (just turn over the pancreas, n=24), AP group (n=24) and AP-EGF group (n=24). Animals in the AP-EGF group were given injections of EGF (0.1 mg.kg-1) subcutaneously post induced AP. Other animals were received the same volume of saline. At 6h, 12h and 24h after induced acute pancreatitis, every 8 animals in each group were sacrificed respectively. 2 ml of blood sample was withdrawn from heart for the analysis of amylase activity in serum. Ascites was sucked with dry gauze and was weighed thereafter. Changes of pancreas shape were evaluated at every time points. The same part of pancreas was used for measurement of MD A content, AI and histologic changes. At the same time, 2 cm of proximal jejunal segment, which was 10 cm distal from the ligament of Treitz, was used to determine AI of jejunum. Another 10 cm segment of jejunum was obtained and the mucosa were scraped for the measurement of MDA content.Results 1. Histologic damage of pancreas in the AP+EGF group was milder as compared with the AP group. 2. Ascites volume in the AP+EGF group decreased significantly as compared with the AP group at 12h and 24h (4.53+1.29vs 6.78+1.47,P<0.05; 7.68+1.85 vs 11.96+2.13, P<0.01, g). Amylase activity in the AP+EGF group also decreased significantly as compared with the AP group on 12h and 24h (142.0+8.3 vs 187.9+10.4, P<0.05;194.3+10.4 vs 253.3+8.6, P<0.01,U). 3. MDA content in plasm (1.85+0.29 vs 2.12+0.27, 2.34+0.23 vs 3.15+0.38, mol.g-1, P<0.05),jejunum (1.18+0.25 vs 1.31+0.24, 1.48+0.32 vs 2.15+0.57, mol. g-1, P<0.05) and pancreas (4.69+1.28 vs 5.13+1.54, 5.21+1.46 vs 7.68+1.63, mol.g-1, P<0.05) in the AP+EGF group decreased significantly as compared with the AP group at 24h. 4. AI of pancreas in the AP+EGF group increased significantly as compared with the AP group after induced AP (16.22+3.53 vs 7.35+1.04, 11.67+2.40 vs 4.81+0.86, 6.38+1.42 vs 1.97+0.21,%,P<0.01). AI of jejunum in the AP+EGF group decreased significantly as compared with the AP group at 12h and 24h (2.15+0.26 vs 4.78+0.39, 5.71+1.34 vs 9.56+ 2.01, %, P<0.01).Conclusion 1. It is a simple method to induce AP through puncturing the biliary-pancreatic duct and intraductal infusion of sodium taurocholate solution. The model is stabilized and ready to be duplicated. It is a crediblemodel for pathogenesis and mechanism of AP. 2. EGF may accelerate the restoration of pathologic damage and alleviate the haemorrhage and edema of pancreas. It may also reduce ascites volume and amylase activity in serum. 3. EGF may depress MDA content in plasm, pancreas and jejunal mucosa so that to lighten oxidative damage. 4. EGF may protect pancreas through abduction of cellular apoptosis, and mitigate jejunum mucosal apoptosis induced by AP.
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