Sun Zhi-gao, Huang Quan-zhi, Xu Cheng-yong, Chen Li-ping
Department of Chinese Medical Acupuncture, Hainan Branch, the PLA General Hospital, Hainan 572013, China.
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2013 Mar;33(3):370-5.
To observe the effects of Shuyu Ningxin Recipe (SNR) on the praxiology and the expressions of hippocampal brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) of model rats with chronic stress-induced depression, thus exploring its anti-depression mechanisms.
Sixty adult SD rats were randomly divided into 6 groups, i.e., the normal control group, the model group, the fluoxetine group, the high dose SNR group, the medium dose SNR group, and the low dose SNR group, 10 in each group. All rats were subjected to establish chronic stress-induced depression model for 21 consecutive days. Except those in the normal control group, rats in the rest groups received gastrogavage from the 22nd day. Mice in the model group were administered with normal saline by gastrogavage. SNR at 25.0, 7.5, and 2.5 g/kg was respectively administered to rats in the high dose SNR group, the medium dose SNR group, and the low dose SNR group by gastrogavage. Fluoxetine suspension (12 mg/kg) was given to rats in the fluoxetine group by gastro-gavage. All medication lasted for 3 successive weeks. The weight, open-field test, and the immobility time in forced swimming test were determined before modeling, 3 weeks (after successful modeling), and 6 weeks (by the end of medication). The expressions of hippocampal BDNF and TrkB were measured after the brain tissues were drawn by the end of the experiment.
Compared with the normal control group, the body weight grew slowly, the behavior index decreased, the immobility time in forced swimming test was prolonged, and the expressions of BDNF and TrkB were weaken in the model group (P <0.05, P <0.01).The body weight increased, the behavior was improved, the immobility time in forced swimming test was shortened, and the expressions of BDNF and TrkB were enhanced in the high dose SNR group and the fluoxetine group by the and of medication, showing statistical difference when compared with the model group (P <0.05, P <0.01).
SNR could exert anti-depression by improving the expression levels of hippocampal BDNF and TrkB.
观察舒郁宁心方对慢性应激性抑郁模型大鼠行为学及海马脑源性神经营养因子（BDNF）及其受体酪氨酸激酶B（TrkB）表达的影响，探讨其抗抑郁机制。
将60只成年SD大鼠随机分为6组，即正常对照组、模型组、氟西汀组、舒郁宁心方高剂量组、舒郁宁心方中剂量组和舒郁宁心方低剂量组，每组10只。所有大鼠连续21天建立慢性应激性抑郁模型。除正常对照组外，其余各组大鼠于第22天开始灌胃给药。模型组大鼠灌胃给予生理盐水。舒郁宁心方高剂量组、舒郁宁心方中剂量组和舒郁宁心方低剂量组大鼠分别灌胃给予25.0、7.5和2.5 g/kg舒郁宁心方。氟西汀组大鼠灌胃给予氟西汀混悬液（12 mg/kg）。所有药物连续给药3周。在造模前、造模3周（造模成功后）和6周（给药结束时）测定大鼠体重、旷场试验及强迫游泳试验中的不动时间。实验结束后取脑组织，测定海马BDNF和TrkB的表达。
与正常对照组比较，模型组大鼠体重增长缓慢，行为学指标降低，强迫游泳试验中不动时间延长，BDNF和TrkB表达减弱（P<0.05，P<0.01）。给药结束时，舒郁宁心方高剂量组和氟西汀组大鼠体重增加，行为改善，强迫游泳试验中不动时间缩短，BDNF和TrkB表达增强，与模型组比较差异有统计学意义（P<0.05，P<0.01）。
舒郁宁心方可通过提高海马BDNF和TrkB表达水平发挥抗抑郁作用。
