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.
背景: 癌症患者伴有抑郁症状的发生率较高，而抑郁 情绪又会通过神经- 内分泌- 免疫网络系统来影响癌症 的发生、发展及转归。.
目的: 探讨小鼠胃癌模型血浆及脑组织中Nesfatin-1 水 平及其在胃癌共病抑郁发病中的作用机制。.
方法: 将18 只615 小鼠随机分为正常对照组（NCG）、 胃癌不合并应激抑郁模型组（GCNS）、胃癌合并应激 抑郁模型组（GCS）。GCNS 组小鼠饲养5 周后于皮下 接种小鼠前胃癌细胞（MFC）建立皮下移植瘤模型， GCS 组给以5 周慢性不可预见应激（CUMS）后，皮下 接种MFC 建立皮下移植瘤模型1 周。用旷场实验、蔗 糖偏好试验、强迫游泳试验（FST）评价小鼠的行为。 分别用酶联免疫吸附法（ELISA）及Western Blot 技术 来检测血浆及脑组织中Nesfatin-1 浓度。.
结果: GCS 组体重增量加显著低于GCNS 组(t = -3.39, p ＜ 0.001)、且GCS、GCNS 两组均低于NCG 组(t = -6.33, p ＜ 0.001; t = -2.94, p=0.01)；旷场试验中GCS 组水平 移动距离小于GCNS 组（t = -2.50, p = 0.025）, 且GCS、 GCNS 两组二者均小于NCG 组（t = -5.87, p ＜ 0.001； t = -3.38, p = 0.004）；GCS 组不动时间长于GCNS 组与 NCG 组(t = 2.56, p = 0.022; t = 3.84, p = 0.002)。中脑、 海马及血浆Nesfatin-1 水平NCG 组与GCS 组均显著高 于GCNS 组，且而GCS 组Nesfatin-1 浓度显著高于正常 对照组，结果均有统计学意义。.
结论: 胃癌不合并应激抑郁小鼠脑组织及血浆 Nesfatin-1 水平降低，CUMS 应激可以引起胃癌小鼠的 抑郁样行为，且可以升高脑组织及血浆Nesfatin-1 水平， 因此Nesfatin-1 可能与胃癌及胃癌相关应激抑郁的发病 有关。.
Keywords: Nesfatin-1; depression; gastric cancer; stress.