The Level of Nesfatin-1 in a Mouse Gastric Cancer Model and Its Role in Gastric Cancer Comorbid with Depression.

Abstract

Background: The incidence of depressive symptoms is higher in cancer patients. And depression can also affect the occurrence, development and outcome of cancer through the neuroendocrine-immune-network system.

Objective: To study the level of Nesfatin-1 in the plasma and brain tissue and its role in the pathogenesis in gastric cancer comorbid with depression using a mouse gastric cancer model.

Methods: 18 mice were randomly divided into the normal control group (NCG), gastric cancer without stress model group (GCNS), and gastric cancer combined with stress model group (GCS). The mice of the GCNS group were inoculated subcutaneously with mouse forestomach carcinoma (MFC) after 5 weeks of nomal feeding to establish a model of subcutaneous transplantation tumor. After 5 weeks of chronic unpredicted mild stress (CUMS) in the GCS group, subcutaneous inoculation of MFC was used to establish a subcutaneous transplantation tumor model for 1 week. Evaluation of mice behavior was performed by open field test, sucrose preference test and forced swimming test (FST). Determination of Nesfatin-1 concentration in plasma and brain tissue was carried out using enzyme linked immunosorbent assay (ELISA) and Western Blot.

Results: The weight increment in the GCS group was significantly lower than that in the GCNS group (t=-3.39, p<0.001). And both GCS and GCNS were lower than the NCG group (t=-6.33, p<0.001; t=-2.94, p=0.01). In the open field test, the horizontal moving distance of the GCS group was less than that of the GCNS group (t=-2.50, p=0.025), and both GCS and GCNS were smaller than the NCG group (t=-5.87, p<0.001; t=-3.38, p=0.004). The dead time of the GCS group was longer than that of the GCNS and the NCG groups (t=2.56, p=0.022; t=3.84, p=0.002). The Nesfatin-1 level in the middle brain, hippocampus and plasma was significantly higher in NCG group and GCS group than in the GCNS group. The concentration of Nesfatin-1 in the GCS group was significantly higher than that in the NCG group.

Conclusions: There is a decrease of Nesfatin-1 level in brain tissue and plasma in mice with gastric cancer without stress. CUMS stress can induce depressive behavior in gastric cancer mice, and increase the level of Nesfatin-1 in brain tissue and plasma. Therefore, Nesfatin-1 may be related to the pathogenesis of gastric cancer stress related depression.