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目的:探讨抑郁模型大鼠海马神经可塑性因子的表达及β-细辛醚对其的影响机制。方法:雄性SD大鼠随机分为正常对照组、模型组、氟西汀组和β-细辛醚组,每组15只。采用慢性轻度不可预见性刺激(CUMS)建立抑郁模型。造模d 2开始,氟西汀组和β-细辛醚组灌胃给药,每日1次(氟西汀组1.2mg·kg~(-1)·d~(-1),β-细辛醚组25mg·kg~(-1)·d~(-1))。实验d1,7,14,21运用敞箱实验与糖水消耗量指标评定大鼠行为学改变。21d实验结束后,采用免疫组织化学方法测定cREB,BDNF,TrkB蛋白表达,实时定量PcR对BDNF,TrkB,CREB进行定量分析。结果:造模d 21后,模型组大鼠的行为学指标相对于对照组明显的降低(JP<0.05),相对于模型组,氰西汀组和β-细辛醚组大鼠的行为学指标显著升高(P<0.05)。免疫组织化学和实时定量PCR检测结果显示:海马区的CREB,BDNF,TrkB的蛋白和基因水平表达增强(P<0.05)。结论:β-细辛醚具有抗抑郁效应,作用机制与调控大鼠海马的神经可塑性因子CREB,BDNF,TrkB的表达与功能相关。
Objective: To investigate the expression of neuroplasticity factor in hippocampus of depression model and the mechanism of β-asarone. Methods: Male SD rats were randomly divided into normal control group, model group, fluoxetine group and β-asarone group, 15 rats in each group. Depression models were established using chronic mild unpredictable stimuli (CUMS). In the beginning of model d 2, fluoxetine group and β-asarone group were given intragastrically once daily (fluoxetine 1.2 mg · kg -1 · d -1, β- Asarone group 25mg · kg -1 (-1) d -1). Experiments d1, 7, 14, 21 used the open-field test and the index of sugar consumption to evaluate the behavioral changes in rats. At the end of 21d, the expressions of cREB, BDNF and TrkB protein were detected by immunohistochemistry, and quantitative analysis of BDNF, TrkB and CREB was performed by real-time quantitative PCR. Results: The behavioral indexes of the model group were significantly lower than those of the control group after model 21 d administration (P <0.05). Compared with the model group, the behavior of the rats in the nicotine and β-asarone groups The index was significantly higher (P <0.05). The results of immunohistochemistry and real-time quantitative PCR showed that the protein and gene expression of CREB, BDNF and TrkB in hippocampus increased (P <0.05). CONCLUSION: β-asarone has antidepressant effect and its mechanism is related to the function of the expression of CREB, BDNF and TrkB in hippocampus of rats.