Objective: To observe the effect of somatostatin on modulation of IL-10 and TGF-beta 1 in acute pancreatitis and investigate the mechanism.
Methods: SD male rats were divided into 3 groups: Group 1, the normal rats as control (n = 6); Group 2, the rats with acute pancreatitis induced by ductual injection with 5% sodium cholate sulfur at the volume of 0.6 ml/kg without any other treatment (n = 8); Group 3, after pancreatitis were induced, the rats were injected hypodermically with somatostatin 3 micrograms/(kg.hr)(n = 6). The animals were killed at 2, 6 and 24 hours after operation (each period n = 7). The blood samples were taken for measurement of IL-10 and TGF-beta 1 (by ELISA). The weight of pancreatic tissue and amylopsin was also observed.
Results: Both IL-10 and TGF-beta 1 in blood of acute pancreatitis increased significantly (P < 0.05). After the injection of somatostatin, IL-10 and TGF-beta 1 were found remarkably decreased at 24 hours postoperation (P < 0.05). No changes of the weight of pancreatic tissue and amylopsin were observed after the injection of somatostatin.
Conclusion: Somatostatin can depress the increase of inflammatory-associated cytokines (IL-10 and TGF-beta 1) that increased remarkably in acute pancreatitis, which is one of the most important reasons why somatostatin cannot relieve pancreatitis.
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