目的：通过行为学和分子生物学方法，探讨二苯乙烯苷对实验性行为绝望老鼠的抗抑郁作用及其机制。方法采用急性和慢性给药方法，通过小鼠悬尾、小鼠强迫游泳、大鼠强迫游泳和大鼠敞箱实验的行为学实验，观察二苯乙烯苷对抑郁症动物模型的行为学影响；采用免疫组织化学观察神经生长因子表达变化。结果急性（给药1 h）给予20、40、60 mg·kg－1二苯乙烯苷均可降低小鼠悬尾和强迫游泳的不动时间（P ＜0．05），连续给药7 d 也可减少大鼠强迫游泳不动时间（P ＜0．05），还可改善慢性应激抑郁模型大鼠的水平和垂直运动得分（P ＜0．05）。免疫组织化学分析表明二苯乙烯苷可逆转慢性应激抑郁模型中神经生长因子的减少（P ＜0．05）。结论二苯乙烯苷具有抗抑郁症作用，该作用可能与提高海马齿状回神经生长因子的表达、增强神经生长因子信号通路有关。%ABSTRACT:Objective To investigate the antidepressant effect of diphenylethylene glucoside and its mechanism of action in experimental model of behavioral despair by using behavioral and molecular biology methods.Methods The tail suspension,forced swimming and open field tests were used to investigate the effect of diphenylethylene glucoside on behavioristics in acute and chronic animal models of depression.The immunohistochemistry was used to detect the changes in the expression of nerve growth factor.Results Acute administration of diphenylethylene gluco-side at doses of 20,40 and 60 mg·kg-1 shortened the immobility time of mice in forced swimming and tail suspension tests(P <0.05).Successive administration of diphenylethylene glucoside for 7 days shortened the immobility time(P <0.05)and improved the locomotor activity in rat model of chronic unpredictable mild stress(CMS)P <0.05.Immunohistochemistry indicated that CMS-in-duced decrease in nerve growth factor expression in the hippocampus was partly reversed by di-phenylethylene glucoside(P <0.05).Conclusion Diphenylethylene glucoside produces an antide-pressant effect and this effect is mediated by the modulation of nerve growth factor signal path-way in the hippocampus.
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