逍遥散对肝郁脾虚证大鼠边缘系统神经元超微结构的影响

Effect of XiaoYaoSan on ultrastructure of neurons in limbic system of rats with liver depression and spleen deficiency syndrome caused by chronic immobilization stress

目的:探讨慢性束缚应激所致肝郁脾虚证大鼠海马CA1区和杏仁核细胞超微结构的变化,明确逍遥散和6-氰基-7-硝喹啉-2,3-双酮(CNQX)对慢性应激所致肝郁脾虚证的保护作用及其机制。方法:将100只雄性SD大鼠随机分为正常组(A组)、假手术组(B组)、模型组(C组)、逍遥散组(D组)、CNQX组(E组)和逍遥散+CNQX组(F组)。C、D、E、F组大鼠通过连续21d慢性束缚应激建立肝郁脾虚证候模型,D、F组大鼠每天束缚前灌服逍遥散5.32g/kg,E、F组大鼠在第1、4、7、10、13、16、19、21d右侧杏仁核区微量注射α-氨基羟甲基恶唑丙酸(AMPA)受体拮抗剂CNQX0.5μl。第22d处死动物,用透射电镜方法观察海马CA1区和左侧杏仁核神经细胞和突触的形态结构。结果:模型组大鼠海马出现了细胞核变形、线粒体嵴模糊,突触结构不清等,正常组、假手术组和给药各组大鼠CA1区未见明显异常;各组大鼠杏仁核均未见明显异常。结论:逍遥散可改善慢性束缚应激导致的海马CA1区超微结构的损伤,其作用机制可能与CNQX一致。

Objective：To observe the ultrastructural changes of neurons in hippocampal CA1 area and amygdale of rats with liver depression and spleen deficiency syndrome caused by chronic immobilization stress（CIS）, discuss protective effect of XiaoYaoSan and CNQX on liver depression and spleen deficiency syndrome and its mechanism.Methods：100 male SD rats were randomly divided into normal control group（A group）,sham-operation group（B group）,model group（C group）,XiaoYaoSan group（D group）,CNQX group（E group）and XaoYaoSan＋CNQX group（F group）. Rats of C,D,E,F groups were restrained 3 hours per day for 21days to establish model of liver depression and spleen deficiency syndrome caused by chronic immobilization stress （CIS）. Xiaoyaosan was administered from the first day to the 21st day before the immobilization in D and F groups. On the lst,4th,7th,10 th, 13th,16st, 19th,21 st day, unilateral intra-amygdala infusion of the AMPA receptor antagonist CNQX （0.5μ l） was administered to rats of E and F groups. Rats were executed on the 22nd day, and the ultrastructural changes of neurons in hippocampai CA1 area and amygdale were observed by transmission electron microscope.Results： Changes in the ultrastructure of hippocampus neurons and synapses were obvious in model group as compared with other groups; no obvious difference was found in amygdales. Conclusion： XiaoYaoSan can improve the ultrastructural damages of neurons in hippocampal CA1 area, its mechanism may be similar with CNQX.