逍遥散对肝郁脾虚证模型大鼠海马CA1区和杏仁核BLA区GluR2阳性细胞数变化的影响

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目的:考察逍遥散和CNQX(6-氰基-7-nitroquinoxa-line-2,3-二酮,AMPA受体的拮抗剂)分别对肝郁脾虚证模型大鼠海马CA1区和杏仁核BLA区GluR2阳性细胞数变化的影响。方法:75只SD雄性大鼠随机等分为正常组、模型组、假手术组、CNQX组和逍遥散组。以21d慢性束缚应激造肝郁脾虚证模型组,在此基础上,运用脑立体定位仪微量注射造CNQX组,除逍遥散组灌胃逍遥散悬液外,其余组均给予相应生理盐水。比较各组海马CA1区和杏仁核BLA区GluR2阳性细胞数变化趋势是否一致。结果:在海马CA1区,正常组、CNQX组和逍遥散组间GluR2阳性细胞数变化均无统计学意义;在杏仁核BLA区,CNQX组由于拮抗AMPA受体,GluR2阳性细胞数最少。其它各组变化趋势与CA1区各组间变化趋势相反,且正常组和逍遥散组比较差异无统计学意义。排除了手术创伤等混杂因子,在海马CA1区和杏仁核BLA区,逍遥散组和CNQX组GluR2阳性细胞数变化趋势均相似。结论:确证逍遥散有1条调节通路和CNQX作用机制相似,通过纠正杏仁核和海马的“兴奋-抑制”失衡,重建稳态,来治疗肝郁脾虚证。 Objective: To investigate the effects of Xiaoyaosan and CNQX (antagonist of 6-cyano-7-nitroquinoxa-line-2,3-dione and AMPA receptor) on the CA1 and ALA BLA GluR2-positive cells. Methods: Seventy-five SD male rats were randomly divided into normal group, model group, sham operation group, CNQX group and Xiaoyao powder group. On the basis of this model, CNQX group was injected with microinjection of brain stereotaxic instrument. In addition to Xiaoyaosan group, Xiaoyao San suspension was perfused, and the other groups were given the corresponding normal saline. The change tendency of GluR2 positive cells in hippocampal CA1 area and amygdala BLA area was compared. Results: In the hippocampal CA1 area, the number of GluR2 positive cells in the normal group, CNQX group and Xiaoyao powder group had no statistical significance. In the amygdala BLA area, the number of GluR2 positive cells was the lowest in CNQX group because of antagonizing AMPA receptor. The trend of other groups was opposite to that of CA1, and there was no significant difference between normal group and Xiaoyaosan group. Excluding confounding factors such as surgical trauma, the trend of GluR2 positive cells in hippocampal CA1 and almond nucleus BLA, Xiaoyaosan and CNQX groups were similar. CONCLUSIONS: It is confirmed that Xiaoyao Powder has one regulation pathway similar to that of CNQX, and it can treat the syndrome of liver depression and spleen deficiency by correcting the “excitement-inhibition” imbalance of amygdala and hippocampus and rebuilding the steady state.
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