温胆汤对精神分裂症模型鼠海马谷氨酸和 N-甲基-D-天冬门氨酸受体亚单位表达的影响

目的:观察温胆汤对精神分裂症模型鼠海马谷氨酸(Glu)和N-甲基-D-天冬门氨酸(NMDA)受体亚单位表达的影响。方法:将30只SD大鼠,随机分3组,每组10只,分别为正常组(A)、模型组(B)及温胆汤组(C),A,B组ig生理盐水20mL.kg-1,C组ig温胆汤20 g.kg-1,每天1次,21 d后地卓西平马来酸盐(MK801)ip诱发精神分裂症,造模3 d后,4℃4%多聚甲醛磷酸盐缓冲液大脑灌注固定、制备脑组织切片,免疫组化染色,观察各组大鼠海马NMDA受体NR1、NR2B亚单位的表达并进行病理评分。结果:正常组评分为"—",模型组评分为13+,温胆汤组为8+。与模型组比较,差异有显著性(P<0.05)。各组大鼠海马NMDA受体NR1、NR2B亚单位的表达存在差异,模型组海马细胞Glu降低,NMDA受体代偿性增高,呈强阳性反应;正常组和温胆汤组呈弱阳性反应的趋势。结论:温胆汤能调节离子型谷氨酸受体的表达水平,对精神分裂症模型鼠海马的病理损伤有一定的保护作用。

Effect of Wendan Decoction on Receptor of Glutamic Acid and N-methyl-D-aspartate in Rats with Schizophrenia

Objective: To explore the effect of Wendan Decoction (WDD) on the receptor of glutamic acid (Glu) and N-methyl-D-aspartate (NMDA ) in rats with schizophrenia. Method: Thirty SD rats were divided randomly into 3 groups with 10 in each group: normal group (A), model group (B) and WDD group (C). WDD group was administered intragatrically with 20 g · kg^-1 WDD;the other groups were administered the same volume of normal saline (20 mL ·kg^-1). The 3 groups were treated for 21 days. Except the normal group, the other groups were given MK801 with sinistro-intraperitoneal injection to set the schizophrenia model after 1 hour of intragastrical administration in the last 3 days. The dosage was 0.1 mL per 20 g. By the changes in immunohistochemistry and neuropathological morphology, we observed the influence of WDD on expression of receptor Glu in hippocampus,receptor subunit NR1 and NR2B of NMDA and protective effects on pathological injuries in hippocampus of the model rats. Result: The morphological observation showed that there were significant differences in expression of Glu, subunit NR1 and NR2B of NMDA receptor in all groups and there also were significant differences in cell structure and cell denaturalization of CA1 area in hippocampus. Conclusion: WDD can improve disorder of cell rearrangement, relieve the process of nuclei dissolution, postpone the denaturalization of hippocampus cell. It indicates WDD has certain protective effects on pathological injury in hippocampus of the model rats.