丹龙醒脑片对血管性痴呆大鼠学习记忆及脑组织兴奋性氨基酸影响的实验研究

目的：探讨血管性痴呆（VD）病理机制并研究丹龙醒脑片（DLXNP）对血管性痴呆大鼠模型脑组织兴奋性氨基酸（EAAs)含量的干预作用。方法：除正常对照组及假手术组外，其余各组大鼠均用双侧颈总动脉反复夹闭再灌注配合腹腔注射硝普钠降压方法建立VD大鼠模型。夹闭2次，每次10min，中间再通10min。用跳台法观察各组大鼠学习记忆功能；用高效液相色谱分析荧光法（HPLC）检测脑组织谷氨酸（Glu)、天门冬氨酸（Asp)浓度。结果：模型组与正常对照组和假手术组相比，跳台实验的错误次数及受电击时间明显增多，潜伏期明显缩短，学习记忆能力降低，Glu、Asp含量明显升高，丹龙醒脑片大、中剂量组与模型组相比：（1）跳台实验的错误次数及受电击时间明显减少，潜伏期明显延长；（2）脑组织中Glu,Asp的含量明显降低。丹龙醒脑片组疗效与尼莫地平组接近。结论：丹龙醒脑片能调节脑组织兴奋性氨基酸含量、减轻其兴奋性毒性，保护大脑神经细胞，这可能是丹龙醒脑片治疗VD的作用机制之一。

An Experimental Study on the Effects of DLXNP on Learningand Memory Ability and Cerebral EAAsin Rat Models of Vascular Dementia

Objective To explore the pathological mechanism of vascular dementia and to investigate DLXNP's intervenient effects on cerebral EAAs. Methods The experimental SD (Sprague-Dauley) rats were divided randomly into 5 groups: normal group, sham operation group, cerebral ischemia reperfusion group, DLXNP group, and nimodipine group. Except animals in the normal group and sham operation one,each of the rats was repeatedly induced lerebral ischemia and reperfused for two times, combined with intraperitoneal injection of sodium nitroprusside to establish the vascular dementia model. Bilateral carotid arteries (CCA) were occluded with artery clips for two times,10 minutes each time, and blood was recirculated for 10 minutes by removal of clips. Set-down avoidance test was used to messure the learning and memory ability.Then, the effects of DLXNP on cerebral excitatory amino acids (EAAs) were detected by HPLC for the samples ertracted from cerebral tissues. Results Compared with the normal group and the sham operation one, the cerebral ischemia reperfusion group's learning and memory ability was significantly decreased, the concentrations of Glu, and Asp were dramatically increased. Compared with the cerebral ischemia reperfusion group,learning and memory ability were increased in the high and middle dosed DLXNP groups, and the contents of Glu, Asp were decreased. The therapeutic effect of DLXNP was similar to that of nimodipine. Conclusion DLXNP has the function of improving learning and memory ability through regulating EAAs and reducing its excitatory nerotoxicity, which may be one of the mechanisms of DLXNP to treat this lesion.