氟西汀对抑郁大鼠模型海马组织BDNF，TrkB表达的影响研究

摘要:目的　研究氟西汀对抑郁大鼠模型海马组织BDNF，TrkB表达的影响。方法　经强度应激方法复制抑郁大鼠模型，随机分成3组:模型对照组、氟西汀干预组（灌胃，4，8 mg/kg，连续30 d），同时增加正常对照组。记录动物体重变化并采用旷场实验评估大鼠精神状况。同时应用免疫组织化学法检测海马组织脑源性神经营养因子（BDNF）表达，以及Western blotting法检测海马组织酪氨酸激酶B（TrkB）蛋白表达。结果　与模型组对照比较，氟西汀明显抑制抑郁大鼠的体重减少并改善其精神状况（P＜0.01）。而海马组织BDNF免疫阳性细胞数量显著增加（P＜0.01），同时增加内源性TrkB蛋白表达（P＜0.01）。结论　氟西汀对抑郁大鼠海马损伤具有神经保护作用，其机制与调节内源性BDNF，TrkB表达而发挥抗抑郁作用有关。

Effect of fluoxetine on BDNF,TrkB expression in hippocampus tissue of depression rat model

Abstract: Objective To study the effect of fluoxetine on BDNF, TrkB expression in hippocampus tissue of depression rat model. Method Depression rat model was induced by chronic stress method, and the animals were randomly assigned in 3 groups: model control group, fluoxetine administration groups (ig, 4, 8 mg/kg, for 30 days). Then, the healthy rats were added as the normal control. The weight change of tested rats was recorded and mental conditions were observed using open-field test. The brain derived neurophic factor (BDNF) expression in hippocampus tissue was determined through immunohistochemistry assay, while the TrkB protein level in hippocampus tissue was measured by western blotting analysis. Result Comparing the two groups, fluoxetine significantly inhibited body weight in depression rats and improved the psychological conditions (P<0.01). The number of BDNF immunoreactive cells in hippocampus tissue notably increased (P<0.01), while endogenous TrkB protein expression elevated (P<0.01). Conclusion The results indicate that fluoxetine exerts neuroprotective effect on impaired hippocampi of depression rat, which is related to regulating endogenous BDNF/TrkB pathway for antidepressant role.