P-mljOR/P70S6K信号通路在急性出血坏死型 胰腺^炎症反应中的调控作用.

Objective To investigate the regulation effect of phosphorylated mammalian target of rapamycin (p-mTOR)/p70 ribosomal protein S6 kinase (p70S6K) signaling pathway in the inflammatory response of acute necrotizing pancreatitis (ANP). Methods Ninety-six male SPF rats were randomly divided into the ANP model group, rapamycin group, and blank control group. The rats in the ANP model group were injected with 1 miykg of 5 % sodium tauroeholate in the opposite direction of pancreatic duct. The rats in the rapamycin group were injected with 0.5 mg/kg rapamycin intra-peritoneally on the basis of the model group. Serum samples were collected from 8 rats in each group at 3, 6, 12, and 24 h after the model was established, and the levels of AMY, TNF-a, IL-6, and IL-10 in the serum were measured. Pancreatic tissues were taken for the detection of p-mTOR and p70S6K protein expression by Western blotting, for histopathological observation by HE staining, and apoptotic index by TUNEL. Results At each time point, the serum levels of AMY, TNF-a, and IL-6 in the rapamycin group were significantly lower than those in the ANP group (all P < 0. 01) , but IL-10 was significantly higher than that of the ANP group (P < 0. 01). All the parameters in the ANP model group and rapamycin group were higher than those of the blank control group (all P < 0. 05). The expression of p-mTOR and p70S6K in the rapamycin group was significantly lower than that in the ANP model group (both P <0. 01). The apoptosis index of the rapamycin group was also significantly lower than that of model group (P <0.01). Histopathological examination showed that the degree of lesions in the pancreatic tissues of the rapamycin group was lighter than that in the model group. Conclusion Decreased activity of p-mTOR/p70S6K pathway can improve inflammation and reduce pancreatic tissue lesions in ANP rats. [ABSTRACT FROM AUTHOR]