Sun Baomin, Lv Yanhua, Xu Hua, Qi Chunhua, Li Cuiping, Liu Pengfei
Department of Psychology, Taian City Central Hospital, Taian, Shandong 271000, P.R. China.
Department of Psychiatry, Taian City Mental Hospital, Taian, Shandong 271000, P.R. China.
Exp Ther Med. 2020 Sep;20(3):2895-2902. doi: 10.3892/etm.2020.9026. Epub 2020 Jul 21.
Effects of Vortioxetine on the expression of brain-derived neurotrophic factor (BDNF) and tyrosine kinase B (Trk B) in hippocampus of depressive rats were investigated. Forty-five SD rats were randomly divided into three groups: model control, Vortioxetine and normal control group, with 15 rats in each group. The changes of body mass were recorded within 5 weeks, and the open field test, sugar water preference test and Morris water maze test were performed to evaluate the behavior and mental status of the rats. The expression of BDNF and Trk B in rat hippocampus was detected by enzyme-linked immuno sorbent assay. Compared with the model control group, the body mass, horizontal and vertical movement, sugar and water preference rate of the vortioxetine group in the 5th week were significantly higher than those of the model control group (P<0.05), and significantly lower than those of the normal control group (P<0.05). The escape latency of the Vortioxetine group within 4 days was significantly lower than that of model control group (P<0.05), but higher than that of normal control group (P<0.05). The target quadrant residence time of the Vortioxetine group was significantly lower than that of the model control group (P<0.05), but higher than that of the normal control group (P<0.05). Expression of BDNF and Trk B in the Vortioxetine group was significantly higher than that in the model control group (P<0.05), but lower than that of the normal control group (P<0.05). Collectively, Vortioxetine can effectively alleviate the symptoms of autonomous and exploratory behavior, and reduce the decrease of learning and memory in depressive rats. Vortioxetine can increase the expression of BDNF and Trk B in depressive rats and alleviate their depressive behavior.
研究了伏硫西汀对抑郁大鼠海马中脑源性神经营养因子（BDNF）和酪氨酸激酶B（Trk B）表达的影响。45只SD大鼠随机分为三组：模型对照组、伏硫西汀组和正常对照组，每组15只。记录5周内大鼠体重变化，并进行旷场试验、糖水偏好试验和Morris水迷宫试验以评估大鼠的行为和精神状态。采用酶联免疫吸附测定法检测大鼠海马中BDNF和Trk B的表达。与模型对照组相比，伏硫西汀组第5周的体重、水平和垂直运动、糖水偏好率均显著高于模型对照组（P<0.05），且显著低于正常对照组（P<0.05）。伏硫西汀组4天内的逃避潜伏期显著低于模型对照组（P<0.05），但高于正常对照组（P<0.05）。伏硫西汀组的目标象限停留时间显著低于模型对照组（P<0.05），但高于正常对照组（P<0.05）。伏硫西汀组中BDNF和Trk B的表达显著高于模型对照组（P<0.05），但低于正常对照组（P<0.05）。总体而言，伏硫西汀可有效缓解抑郁大鼠的自主和探索行为症状，并减少其学习和记忆能力的下降。伏硫西汀可增加抑郁大鼠中BDNF和Trk B的表达并减轻其抑郁行为。
