中文摘要：

本文研究了三七叶总皂苷的抗抑郁作用及其作用机制。40只大鼠随机分成空白组、模型组、氟西汀组和三七叶总皂苷中高剂量组,建立慢性应激抑郁大鼠模型评价三七叶总皂苷的抗抑郁活性以及对海马体cAMP、PKA、BDNF的影响。建模四周后,模型组大鼠与空白组比较,体重、糖水偏好率及自主活动水平等行为学指标分别降低了8.56%、22.48%、26.17%,表现出人类抑郁症中体重下降、快感缺失、自主活动下降等核心症状,而大鼠海马体cAMP、PKA、BDNF的水平分别降低了53.60%、53.60%、39.20%。给予三七叶总皂苷治疗后,与模型组相比,三七叶总皂苷高剂量组大鼠上述三个行为学指标分别增加了7.03%、26.21%、26.21%,上述三个生化指标也分别升高了41.29%、62.79%、49.05%。表明三七叶总皂苷能逆转抑郁大鼠行为学症状以及调节海马体cAMP、PKA、BDNF的水平。三七叶总皂苷具有良好的抗抑郁作用,其作用机制与调控海马体cAMP、PKA、BDNF水平有关。

英文摘要：

This study evaluated the antidepressant effects and corresponding mechanism of the total saponins in leaves of Panax notoginseng（TSLPN）. A chronic unpredictable mild stress（CUMS） rat model of depression was established to evaluate the antidepressant effects of TSLPN and the effects of TSLPN on the levels of cyclic adenosine monophosphate（cAMP）, protein kinase A（PKA）, brain-derived neurotrophic factor（BDNF） in thehippocampus of rats. Forty rats were randomly divided into five groups： control, CUMS, fluoxetine, medium dosage of TSLPN, andhigh dosage of TSLPN groups. After exposure to CUMS for four weeks, compared with the rats in control group, those in CUMS group showed decreases in three behavioral indices-body weight, sucrose preference, and locomotor activity by 8.56%, 22.48%, and 26.17%, respectively. Animals exhibited depression-like symptoms, such as loss in body weight, anhedonia, and decrease in locomotor activity, and the levels of cAMP, PKA, BDNF in thehippocampus also decreased by 53.60%, 53.60%, and 39.20%, respectively. After TSLPN treatment, compared with CUMS group, the above-mentioned three behavioral indices of the rats inhigh dosage TSLPN increased by 7.03%, 26.21%, and 26.21%, respectively; the levels of three biochemical indices–cAMP, PKA, and BDNF levels–also increased by 41.29%, 62.79%, and 49.05%, respectively. These results indicated that TSLPN could reverse the depression-like behaviors and regulate the levels of cAMP, PKA, and BDNF in thehippocampus. In conclusion, TSLPN was found tohave excellent antidepressant effects, and its functioning mechanism was related to the regulation of cAMP, PKA, and BDNF levels in thehippocampus.