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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 investigate the ultrastructural changes of hippocampal CA1 and amygdala in chronic obstructive stress-induced rats with liver-qi and spleen-deficiency syndrome. To clarify the changes of ultrastructure of hippocampal CA1 and amygdala in rats, CNQX) on chronic stress-induced liver-spleen-deficiency syndrome and its mechanism. Methods: 100 male SD rats were randomly divided into normal group (A group), sham operation group (B group), model group (C group), Xiaoyao powder group (D group), CNQX group (E group) Casual + CNQX group (F group). Rats in groups C, D, E and F were challenged by chronic restraint stress for 21 days. The rats in groups D and F were fed with Xiaoyaosan 5.32g / kg daily before shackling. Rats in groups E and F were challenged with On the 1st, 4th, 7th, 10th, 13th, 16th, 19th and 21st day, the right amygdala was injected with 0.5 μg of α-Aminomethylol oxazole propionic acid (AMPA) receptor antagonist CNQX. The animals were sacrificed on the 22nd day, and the morphology of neurons and synapses in the hippocampal CA1 and left amygdala were observed by transmission electron microscopy. Results: The hippocampus of rats in model group showed nuclear deformation, fuzzy mitochondrial cristae and unclear synaptic structure. There was no obvious abnormality in CA1 area of normal group, sham operation group and administration group. No obvious abnormalities. Conclusion: Xiaoyao powder can improve the ultrastructural damage induced by chronic restraint stress in hippocampal CA1 region. The mechanism may be consistent with CNQX.