关键词: PI3K/AKT/mTOR通路, 急性胰腺炎, 胃肠功能障碍

Abstract: Objective To investigate whether activation of PI3K/AKT/mTOR pathway can reduce inflammation in acute pancreatitis (AP) rats. Methods SD rats were grouped into sham surgery group, model group, Gln group, and Gln+LY294002 group (PI3K/AKT/mTOR pathway inhibitors). Intra-abdominal pressure (IAP), ascites volume(AS), serum amylase (AMY), diamine oxidase (DAO), interleukin(IL-1β, IL-6), Tumor necrosis factor (TNF-α) were measured. The pathological change in pancreatic and small intestinal tissues was evaluated by microscopy; The expression of PI3K, Akt and mTOR genes and cytoplasm compact linking protein (ZO-1), compact linking protein (occludin-1), PI3K, Akt and mTOR in ileum of each group were detected. Results Compared with the sham surgery group, the IAP and AS, IL-1β, IL-6, TNF-α, AMY, DAO, and pathological injury scores of pancreas and small intestine in the model group were obviously increased; The expression of PI3K mRNA,Akt mRNA, mTOR mRNA, ZO-1, occludin-1, p-PI3K/PI3K, p-Akt/Akt and p-mTOR/mTOR in rat ileum tissue significantly reduced (P＜0.05). Compared with the model group, the level of IAP and AS, IL-1β, IL-6, TNF-α, AMY, DAO and pathological injury scores of pancreas and small intestine in the Gln group were significantly reduced; The expression of PI3K mRNA, Akt mRNA, mTOR mRNA, ZO-1, occludin-1, p-PI3K/PI3K, p-Akt/Akt and p-mTOR/mTOR in rat ileum tissue was significantly increased (P＜0.05); LY294002 could specifically reverse the therapeutic effect of Gln on acute pancreatitis in rats. Conclusions Activation of PI3K/AKT/mTOR pathway may reduce inflammation and improve gastrointestinal function in rats with acute pancreatitis.

Key words: PI3K/AKT/mTOR pathway, acute pancreatitis, gastrointestinal dysfunction