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目的:探讨三七总皂苷(total saponins of Panax notoginseng，TSPN)对卒中后抑郁(post stroke depression，PSD)模型大鼠学习记忆的影响及其作用机制。方法:采用四血管阻断法制作大鼠卒中模型，7 d后采用社会隔离＋慢性不可预见性温和应激(CUMS)方法制备PSD模型。大鼠被随机分成假手术组(Sham组，n n＝10)、卒中组(Model组，n n＝10)、卒中后抑郁组(PSD组，n n＝10)和PSD＋三七总皂苷组(TSPN组，n n＝10)。Model组和PSD组在脑缺血后30 min腹腔注射等体积生理盐水，1次/d；TSPN组给予PSD大鼠腹腔注射剂量为75 mg/kg的TSPN，1次/d，连续30 d。30 d后采用水迷宫实验检测各组大鼠的学习记忆，免疫印迹技术检测海马微管相关蛋白(DCX)和巢蛋白(Nestin)的表达，免疫荧光观察海马齿状回的颗粒下层(SGZ)区DCX与内源性细胞增殖标记物(Ki67)的共表达。n 结果:与Sham组、Model组相比[(10.4±3.2) s、(19.8±3.7) s]，PSD组在第5天的逃避潜伏期[(31.8±3.8) s]显著延长(n t＝9.23，5.15；均n P<0.05)；给予TSPN干预后，大鼠的逃避潜伏期[(14.2±2.8)s]较PSD组明显缩短(n t＝8.56，n P<0.05)。与Sham组相比[(10.3±1.7)次]，PSD组跨越平台次数[(4.1±1.1)次]显著减少(n t＝11.24，n P<0.05)，给予TSPN干预后PSD大鼠跨越平台次数[(8.4±1.6)次]显著增加(n t＝5.77，n P<0.01)。PSD组海马DCX、Nestin的蛋白水平分别为(0.60±0.02)、(0.58±0.03)，给予TSPN干预之后，PSD大鼠海马DCX、Nestin的蛋白水平显著升高(1.07±0.07)、(0.95±0.11)，两组DCX、Nestin的蛋白水平的差异有统计学意义(n t＝20.22，7.68；均n P<0.01)。PSD组大鼠海马SGZ区DCX/Ki67细胞为(16.2±2.8)个/mmn 2，TSPN组为(21.2±3.1)个/mmn 2，差异有统计学意义(n t＝2.42，n P<0.05)。n 结论:三七总皂苷可通过促进海马神经再生改善卒中后抑郁大鼠的学习记忆。“,”Objective:To investigate the effect of total saponins of Panax notoginseng (TSPN) on learning and memory of post-stroke depression (PSD) rats and its mechanism.Methods:Four-vessel occlusion method was used to build the rat stroke model and 7 days later these rats were given solitary breeding with chronic unpredictable mild stress (CUMS) to make depression model. Rats were randomly divided into Sham group (n n=10), Model group (n n=10), PSD group (n n=10) and TSPN group (n n=10). The rats in the Model group and PSD group were injected administered with equal volume of 0.9% saline 30 min post-brain ischemia, one injection per day for 30 days. while TSPN group were treated with TSPN. The dose of TSPN (75 mg/kg) was dissolved in 0.9% saline 10 g/L, once per day for 30 days. Then the learning and memory of rats were tested by Morris water maze.The protein levels of DCX and Nestin in the hippocampus were detected by Western blot. Furthermore, the DCX/Ki67 co-labeled cells in the SGZ of hippocampus were observed by the immunofluorescence.n Results:The escape latency at the fifth day of PSD group((31.8±3.8)s) was longer than that in the Sham group((10.4±3.2)s) and Model group((19.8±3.7)s) ( n t=9.23, 5.15; both n P<0.05). The escape latency ((14.2±2.8)s) of TSPN group was shortened significantly than PSD group (n t=8.56, n P<0.05). The times across the platform in the Sham group was (10.3±1.7), and the PSD group was (4.1±1.1), difference was statistically significant between two groups(n t=11.24, n P<0.05). The times across the platform (8.4±1.6) of TSPN group statistically increased compared with PSD group (n t=5.77, n P<0.05). The protein levels of DCX and Nestin in the PSD group were (0.60±0.02), (0.58±0.03) respectively, and in the TSPN group were (1.07±0.07), (0.95±0.11) correspondingly, there were significant differences of the DCX, Nestin protein level between the two groups(n t=20.22, 7.68, both n P<0.01). Moreover, there was significant difference in the number of the DCX/Ki67cells in the hippocampus SGZ between the PSD group((16.2±2.8) /mmn 2) and TSPN group ((21.2±3.1) /mmn 2)(n t=2.42, n P<0.05).n Conclusion:TSPN could improve the learning and memory of the rats with post-stroke depression through enhancing the hippocampus neurogenesis.