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作 者:荣华[1] 高志影[1] 韩丽君[1] 赵春明[1] 刘得水[1] 张晓杰[1]
出 处:《中国新药杂志》2016年第10期1186-1190,共5页Chinese Journal of New Drugs
基 金:黑龙江省自然科学基金资助项目(H201354)
摘 要:目的:探讨抑郁模型大鼠海马神经突触可塑性因子GAP-43的表达及β-细辛醚对其的影响机制。方法:雄性SD大鼠随机分为空白对照组、模型组、盐酸氟西汀组、β-细辛醚低剂量组及β-细辛醚高剂量组,每组各20只。采用慢性轻度不可预见性刺激(CUMS)建立抑郁模型。实验7 d后,于造模同时,各组灌胃给药,qd(盐酸氟西汀组10 mg·kg^(-1)·d^(-1),β-细辛醚低剂量组25 mg·kg^(-1)·d^(-1),β-细辛醚高剂量组50 mg·kg^(-1)·d^(-1))。实验d 1,d 7,d 14,d 21,d 28运用敞箱实验(open-field-test)与糖水消耗量指标评定大鼠行为学改变。28 d实验结束后,采用免疫荧光标记技术检测GAP-43蛋白表达,实时定量PCR技术对GAP-43mRNA表达进行定量分析。结果:实验28 d后,模型组大鼠的行为学指标相对于空白对照组明显的降低(P<0.05),相对于模型组,盐酸氟西汀组和β-细辛醚低剂量组和β-细辛醚高剂量组大鼠的行为学指标显著升高(P<0.05)。免疫荧光标记和实时定量PCR检测结果显示:β-细辛醚低高剂量组大鼠海马区的GAP-43蛋白和mRNA水平表达降低(P<0.05)。结论:β-细辛醚具有抗抑郁效应,其作用机制与调控大鼠海马神经突触可塑性功能因子GAP-43的表达与功能相关。Objective: To investigate the effect of β-asarone on the expression of synaptic plasticity factors in hippocampal in a rat model of depression. Methods: Male Sprague-Dawley rats were randomly divided into groups( n = 20 in each group). They were exposed to chronic unpredictable mild stress( CUMS) to induce depression,and treated with fluoxetine hydrochloride( 10 mg·kg^(- 1)·d^(- 1)) or β-asarone( 25 and 50 mg·kg^(- 1)·d^(- 1)).The sucrose consumption and open-field-test were assessed to evaluate behavioral changes at 1,7,14,21 and 28 days,respectively. After the experiment of 28 days,the expression of GAP-43 was detected by immunofluorescence and real-time quantitative PCR. Results: At 28 days,the behavioral indexes reduced in depression control group compared with normal control group( P 〈0. 05). The reduced behavioral indexes were significantly increased byβ-asarone( P 〈0. 05). Results of immunofluorescence test and real-time quantitave PCR analysis showed that thehippocampal expression of GAP-43 significantly decreased in rats treated with β-asarone( P 〈0. 05). Conclusion:β-Asarone can effectively relieve depression in rats,which may be related to regulation of hippocampal synaptic plasticity.
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