目的：探讨β-细辛醚对抑郁模型大鼠海马CA3区超微结构及脑组织ERK蛋白表达的影响及干预作用。方法：选取60只4~5月龄SD雄性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应激制作大鼠抑郁模型，造模第2天开始，氟西汀组和β-细辛醚组给予氟西汀和石菖蒲干预，于实验第1、7、14、21天，分别进行体重、糖水偏爱度检测和敞箱实验，对大鼠行为学改变进行评定。采用电镜技术观察大鼠大脑组织海马CA3区超微结构的改变，采用免疫组织化学染色和计算机图像分析技术测定检测ERK蛋白阳性目标积分光密度及其表达的变化。结果：电镜观察结果显示：模型组大鼠海马神经元凋亡增加，β-细辛醚能改善大鼠海马病理改变；免疫组化结果显示：与模型组比较，氟西汀组和β-细辛醚组大鼠行为学指标显著改善，海马区ERK蛋白表达增强，差异有统计学意义（P<0.05）。结论：β-细辛醚可显著改善抑郁模型大鼠的抑郁症状，其作用机制可能与增强ERK蛋白表达有关。%Objective:To observe the effect of beta-asarone on CA3 ultrastructure in hippocampus and the expression of ERK protein in the hippocampus of depression model rats. Method:4-5 month old 60 male Sprague-Dawley rats were randomly divided into normal control group,model control group,β-asarone group,fluoxetine control group,each group contained 15 rats. 21 d accepted chronic unpredictable mild stress. From the second day,Western medicine and Chinese medicine were given fluoxetine at the same time andβ-asarone intervention. On the 1,7,14,21th day,open-field experiments,detection of sugar consumption and body weight were detected respectively in rats as assessed by indicators such as detection of behavior change. Change of hippocampus was observed by electron microscope. Protein ERK expression in brain tissue was assayed by immunohistochemical test and computer image analysis technology. Result:Number of apoptotic cells of hippocampal CA3 area in model control group were found increased,andβ-asarone could alleviate the damage of hippocampus neurons. Compared with the model control group,the protein expressions of ERK in the hippocampus inβ-asarone group and fluoxetine group increased with statistical significance(P<0.05). Conclusion:Beta-asarone can obviously improve the depressive state of the model rats. Its mechanism might be related with increasing the protein expressions ERK and reducing the brain neural cell apoptosis.
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