Abstract: Objective To investigate the effects of ulinastatin (UTI) combined with somatostatin (SOM) on intestinal damage in acute pancreatitis (AP) rats and the possible mechanisms of action. Methods The rats were randomly divided into sham-operated (sham) group, AP group, UTI group, UIT+SOM group and UIT+SOM+JAK2 activator (CA1) group, 15 rats/group, respectively. Twelve hours after administration, the intestinal permeability, serum biochemical indicators, and inflammatory factor of rats were detected. HE staining was applied to observe the pathological changes in pancreatic and intestinal tissues. TUNEL method was applied to detect apoptosis in intestinal tissue. Western blot was applied to detect the expression of JAK2/STAT3 signaling pathway proteins. Results Compared with the sham group, the pancreatic tissue of rats in the AP group showed obvious inflammatory cell infiltration, edema and bleeding, while the intestinal mucosa showed inflammatory cell infiltration, irregular villi, shedding and necrosis of intestinal epithelial cells in the intestinal tissue. The intestinal permeability, serum amylase (AMY), lipase(LIPA) activities, diamine oxidase (DAO) activities, tumor necrosis factor α(TNF-α), interleukin-6(IL-6) level, pancreatic and intestinal histopathological scores, intestinal tissue cell apoptosis rate, and p-JAK2/JAK2, p-STAT3/STAT3 ratio all significantly increased (P＜0.05). Compared with the AP group, the pancreatic and intestinal tissue injury of rats in the UTI group and UIT+SOM group was reduced, and inflammatory cell infiltration was reduced. The intestinal permeability, serum AMY, LIPA activities, DAO activities, TNF-α, IL-6 level, pancreatic and intestinal histopathological scores, intestinal tissue cell apoptosis rate and p-JAK2/JAK2, p-STAT3/STAT3 ratio were all decreased (P＜0.05). The pancreatic and intestinal tissue injury of rats in the UIT+SOM+CA1 group were more severe, and the trends of the above indicators were opposite to those found in UIT+SOM group (P＜0.05). Conclusions The combination of UTI and SOM attenuated intestinal injury in AP rats, and potential mechanism may involve in the inhibition of the JAK2/STAT3 signaling pathway.

Key words: ulinastatin, somatostatin, acute pancreatitis, intestinal injury, JAK2/STAT3