目的 探討人參次苷H滴丸對慢性溫和不可預(yù)見性應(yīng)激結(jié)合孤養(yǎng)方法建立抑郁模型大鼠的抗抑郁作用及其作用機(jī)制。方法 96只大鼠隨機(jī)分為對照組、模型組、氟西汀組和人參次苷H滴丸28、56、112 mg/kg組，每組16只。除對照組外各組分別孤養(yǎng)并接受5周慢性溫和不可預(yù)見性應(yīng)激刺激造模。同時(shí)氟西?。?0 mg/kg）組、人參次苷H滴丸28、56、112 mg/kg組ig給藥，對照組、模型組ig相應(yīng)體積（10 mL/kg）純水。對大鼠體質(zhì)量變化、糖水消耗比、敞箱實(shí)驗(yàn)行為學(xué)評分進(jìn)行比較，對血漿皮質(zhì)酮（CORT）、皮層、海馬區(qū)神經(jīng)營養(yǎng)因子（BDNF）、5-羥色胺（5-HT）、多巴胺（DA）、去甲腎上腺素（NE）水平變化進(jìn)行檢測。尼氏染色后觀察海馬CA1、CA3區(qū)神經(jīng)元數(shù)目和形態(tài)。結(jié)果 與模型組比較，人參次苷H滴丸56、112 mg/kg組體質(zhì)量顯著升高（P< 0.05），人參次苷H滴丸28、56、112 mg/kg組糖水消耗比顯著升高（P< 0.01）；敞箱實(shí)驗(yàn)中人參次苷H滴丸56 mg/kg組大鼠水平運(yùn)動(dòng)得分顯著提高（P< 0.05），56、112 mg/kg組垂直運(yùn)動(dòng)得分顯著提高（P< 0.05、0.01）；人參次苷H滴丸28、56、112 mg/kg組大鼠血漿CORT水平均有所降低，但差異并無統(tǒng)計(jì)學(xué)意義；人參次苷H滴丸56 mg/kg組皮層、海馬BDNF水平顯著升高（P< 0.05），人參次苷H滴丸56、112 mg/kg組大鼠皮層、海馬5-HT水平顯著升高（P< 0.05、0.01）；人參次苷H滴丸28、56 mg/kg組大鼠皮層、海馬DA水平顯著升高（P< 0.05、0.01）；人參次苷H滴丸28、56、112 mg/kg組大鼠皮層、海馬NE水平升高十分顯著（P< 0.01）。人參次苷H滴丸28、56、112 mg/kg組海馬CA1、CA3區(qū)錐體細(xì)胞形態(tài)較為規(guī)則，排列較為松散，錐體細(xì)胞數(shù)量相對增多。結(jié)論 人參次苷H滴丸具有抗抑郁作用，其作用機(jī)制可能是通過改善抑郁大鼠腎上腺軸功能亢進(jìn)癥狀，提高模型大鼠皮層與海馬5-HT、DA、NE水平，上調(diào)BDNF表達(dá)，以及抑制海馬CA1、CA3區(qū)神經(jīng)元錐體細(xì)胞的凋亡。

Objective To investigate the antidepressant effect of Secondary Ginsenoside H Driping Pills on chronic unpredictable mild stress rats, and explore its mechanisms. Methods SD rats (96) were divided into control group, model group, fluoxetine group, and Secondary Ginsenoside H Driping Pills (28, 56, and 112 mg/kg) groups, and each group had 16 rats. Rats in each group were given social isolation and chronic unpredictable mild stress (CUMS) for 5 weeks to establish models except the control group. At the same time, rats in the fluoxetine (10 mg/kg) group and Secondary Ginsenoside H Driping Pills (28, 56, and 112 mg/kg) groups were ig administered with drugs, while rats in the control group and model group were ig corresponding volume (10 mL/kg) pure water. The body weights, sucrose consumption ratio, and open field test scores were compared. The plasma corticosterone (CORT), brain derived neurotrophic factor (BDNF), serotonin (5-HT), dobaamine (DA), norepinephrine (NE) levels in the hippocampus and frontal cortex were detected. After Nissl staining, the number and morphology of neurons in CA1 and CA3 regions of hippocampus were observed. Results Compared with the model group, body weights in Secondary Ginsenoside H Driping Pills (56 and 112 mg/kg) groups were significantly increased (P < 0.05), and sucrose consumption ratios in Secondary Ginsenoside H Driping Pills (28, 56, and 112 mg/kg) groups were significantly decreased (P < 0.01). Horizontal movement scores in Secondary Ginsenoside H Driping Pills (56 mg/kg) group improved significantly (P < 0.05), and vertical motion scores in Secondary Ginsenoside H Driping Pills (56 and 112 mg/kg) groups also improved significantly (P < 0.05, 0.01). The plasma levels of CORT in Secondary Ginsenoside H Driping Pills (28, 56, and 112 mg/kg) groups were decreased, but the difference was not statistically significant. Cortex and hippocampus BDNF levels in Secondary Ginsenoside H Driping Pills (56 mg/kg) group were increased significantly (P < 0.05); cortex and hippocampus 5-HT levels in Secondary Ginsenoside H Driping Pills (56 and 112 mg/kg) groups were increased significantly (P < 0.05, 0.01); cortex and hippocampus DA levels in Secondary Ginsenoside H Driping Pills (28 and 56 mg/kg) groups were significantly increased (P < 0.05, 0.01); and cortex and hippocampus NE levels in Secondary Ginsenoside H Driping Pills (28, 56, and 112 mg/kg) groups were increased significantly (P < 0.01). The pyramidal cells in CA1 and CA3 regions of the hippocampus in Secondary Ginsenoside H Driping Pills (28, 56, and 112 mg/kg) groups were more regular, loosely arranged, and the number of pyramidal cells increased relatively. Conclusion Secondary Ginsenoside H Driping Pills have antidepressant effect, and the mechanism may be related to improve the symptoms of adrenal axis hyperfunction, improve cerebral cortex and hippocampus 5-HT, DA, and NE levels, up-regulate the expression of BDNF, and inhibit apoptosis of pyramidal neurons in CA1 and CA3 regions of hippocampus.