关键词: 抑郁; 卒中后; 神经生长因子; 氟西汀; 大鼠

Abstract: Objective To observe brain-derived neurotrophic factor levels in the hippocampus of the animal model of post-stroke depression.Methods The focal cerebral ischemia model was set up by blocking the middle cerebral artery(MCA), and then the model rats were separately raised and put into chronic unpredictable mild stress to induce the PSD model, part of them were intervened by fluoxertine. The rats were examined dynamically by Open-field test (OFT), sucrose consumption test. Western-blot and Real time-PCRwere used to detect BDNF protein and mRNA levels respectively.Results On the 14th day after CUMS, the PSD group showed significantly less locomotor activity and sugar-water consumption (P <0.05 or P <0.01) compared with the control group. On the 18th ,28th day, BDNF protein levels of the PSD group declined significantly (P <0.05 or P <0.01) compared with the control group. BDNF mRNA levels on the18th day were reduced, but there was no statisticdifference. While on the 28th day, BDNF mRNA levels significantly declined (P <0.01). On the 14th and 18th day, open-field activities and the amount of sugar-water consumption of the fluoxertin intervention group increased markedly (P <0.05 or P <0.01) compared with the PSD group, while onthe 18th and 28th day, BDNF protein and mRNA levels of the fluoxetine group were significantly increased (P <0.01) compared with the PSD group respectively.Conclusion Anhedonia and underactivity, the core symptoms of depression, exist persistently in the PSD group rats. Fluoxetine may can improve the behavior abnormality of the PSD rats. Brain derived neurotrophic factor levels in the animal model of post-stroke depression was significantlyreduced and fluoxetine can reverse its expression levels, BDNF may has neuroprotect effect in poststroke depression.

Key words: Post stroke depression; Nerve growth factors; Fluoxetine; Rats