中文摘要：

目的建立慢性应激抑郁模型大鼠,观察五乙酰栀子苷对慢性轻度不可预见性应激（CUMS）大鼠抑郁样行为及其对下丘脑-垂体-肾上腺（HPA）轴的影响。方法 60只大鼠随机分为正常组、模型组、五乙酰栀子苷组（25、50、100mg/kg）和氟西汀组（10 mg/kg）。除正常组外,均采用CUMS制备大鼠抑郁模型。从造模第8天开始,五乙酰栀子苷和氟西汀连续灌胃给药2周。糖水偏爱实验、旷场实验及强迫游泳实验检测大鼠行为学,检测血清皮质酮（CORT）、肾上腺指数及下丘脑促肾上腺皮质激素释放激素（CRH）mRNA,探讨五乙酰栀子苷的抗抑郁作用及机制。结果与正常组相比,CUMS大鼠表现出异常行为学及HPA轴活化,五乙酰栀子苷能逆转CUMS诱导的大鼠行为学改变,包括提高糖水消耗量、增加穿格数和站立数、缩短不动时间及延长游泳时间。同时,五乙酰栀子苷能使CUMS大鼠异常的HPA轴功能恢复,包括降低血清CORT和肾上腺指数、抑制下丘脑CRH mRNA表达。结论五乙酰栀子苷可以改善CUMS大鼠行为学,其抗抑郁作用可能与调节HPA轴功能有关。

英文摘要：

Objective To observe the effect of penta-acetyl geniposide on chronic unpredictable mild stress （CUMS） -induced depressive behaviors and its effect on hypothalamic-pituitary-adrenal （ HPA） axis in rats with CUMS-induced depression. Methods Sixty rats were randomly divided into six groups normal group, C U M S group,penta-acetyl geniposide（25 , 50, 100 mg/kg）-treated groups and fluoxetine（ 10 mg/kg）-treated group. Ex-cept the rats in normal group, CUMS was applied to induce depression in rats. Penta-acetyl geniposide and fluoxe-tine were intragastric administrated from day 8 to day 21 after CUMS exposure. Sucrose preference test, open field test and forced swimming test were used to evaluate the antidepressant effect of penta-acetyl geniposide. Corticoster-one （ CORT） serum level, adrenal index and hypothalamic corticotrophin-releasing hormone （ CRH） mRNA level were assayed to assess the potential effect of penta-acetyl geniposide on HPA axis. Results Compared with the nor-mal group, CUMS rats showed abnormal behaviors and HPA axis activation. Penta-acetyl geniposide could reverse the CUMS-induced behavioral abnormalities, as indicated by increased sucrose consumption, improved crossing and rearing behavior, reduced immobility time and increased swimming time. In addition, penta-acetyl geniposide could restore the CUMS-induced overactivity of HPA axis, evidenced by decreased CORT serum level, adrenal gland in-dex and hypothalamic CRH mRNA level. Conclusion Penta-acetyl geniposide can improve the behaviors of CUMS rats and exert its antidepressant effect by modulation of the HPA axis.