Jiang Hua, Li Fei, Liu Shuang, Sun Haichen, Cui Yeqing, Wu Yanchuan, Gao Chongchong
Department of General Surgery, Xuan Wu Hospital of Capital Medical University, China.
Department of General Surgery, Xuan Wu Hospital of Capital Medical University, China.
Pancreatology. 2015 May-Jun;15(3):281-5. doi: 10.1016/j.pan.2015.03.002. Epub 2015 Mar 10.
Acute pancreatitis (AP) has an effect on both inflammatory/autoimmune processes and psychological states, but the pathophysiological causes of pancreatic encephalopathy in the brain are unclear. We hypothesized that the peripheral immune/inflammatory response during AP can affect indolamine 2,3-dioxygenase (IDO) expression and serotonin content in the brain.
About 210 male Sprague Dawley rats were randomly divided into five groups: control (0 h) and 6 h, 24 h, 48 h and 72 h experimental groups. Acute pancreatitis was induced by an injection of a sodium taurocholate solution via a cannulated bile-pancreatic duct. We measured the plasma TNF-α and IL-6 levels; serotonin, 5-HIAA and the protein concentration levels of IDO and monoamine oxidase A (MAO-A) were evaluated in the striatum, hippocampus and left prefrontal cortex.
The IL-6 and the TNF-α levels increased in the 24 h, 48 h and 72 h groups. The IDO concentrations of both the 72 h group in the hippocampus and 48 h, 72 h groups in the prefrontal cortex increased; in the corpus striatum, the IDO concentrations fluctuated without statistical significance. The MAO-A protein concentration of the 6 h and 24 h groups decreased in the striatum, hippocampus and prefrontal cortex. There were no statistically significant differences found in the serotonin and 5-HIAA concentrations.
During the process of AP, cytokines, such as IL-6 and TNF-α, may play a role in activation of neuronal pathways utilizing the metabolic enzyme IDO, which may play an important role in determining the mental symptomatology accompanying AP.