醒脑静对脑缺血大鼠神经保护作用与氨基酸受体表达的关系

Effect of xingnaojing in protecting ischemic rat nerves and its relation with the expression of N-methyl-D-aspartic acid receptor

目的:探讨醒脑静对局灶性脑缺血大鼠海马N-甲基-D-天冬氨酸(NMDA)受体的影响。方法:采用线栓法制备大鼠左侧大脑中动脉阻断(MCAO)模型,分别观察醒脑静对MCAO大鼠神经功能缺损评分、脑梗死体积和海马NMDA受体的含量的影响。结果:缺血3和6h,醒脑静组神经功能缺损评分明显低于MCAO组(P<0.01);且模型组梗死体积24h(197.60±34.03)mm3明显大于6h(140.60±14.81)mm3,差别有统计学意义(P<0.05);但治疗组梗死体积6h是(114.60±23.62)mm3,24h是(125.60±20.51)mm3,后者明显小于模型组(P<0.01);缺血1,6,24h,模型组NMDA受体表达分别为(8.40±1.23),(12.08±1.80),(17.94±1.62)nmol/g,呈逐渐上调趋势(P<0.05),24h时治疗组NMDA受体表达为(5.22±1.43)nmol/g,明显低于模型组(P<0.01)。结论:醒脑静对局灶性脑缺血大鼠具有明确的神经保护作用,其机制可能与拮抗兴奋性氨基酸受体表达上调有关。

AIM:To explore the effect of xingnaojing on N-methyl-D-aspartic acid(NM DA) receptor in hippocampus of focal cerebral ischemic rats. METHODS:Rat left middle cerebral artery was ligated with thread occlusion met hods to establish the cerebral ischemic model of middle cerebral artery occlusio n(MCAO).The effects of xingnaojing on the neurological impairment,volume of cere bral infarction and content of NMDA receptors in the hippocampal region in MCAO rats were detected. RESULTS:The scores of the neurological impairment were significantly lower in the treatment group than those in the model group after ischemia for 3 and 6 h. In the model group,the volume of cerebral infarction at 24 h was(197.60± 34.03) mm3,significantly bigger than that at 6 h[(140.60± 14.81) mm3](P< 0.05).While in the treatment group,the volume of cerebral infarction was(114.60± 23.62) mm3 at 6 h and (125.60± 20.51) mm3 at 24 h,and the latter was significantly smalle r than that of the model group (P< 0.01).The expression of NMDA receptor in the model group was(8.40± 1.23) nmol/g at 1 h,(12.08± 1.80) nmol/g at 6 h and(17.9 4± 1.62) nmol/g at 24 h,which had a tendency to increase(P< 0.05).At 24 h,the e xpression of NMDA receptor in the treatment group was(5.22± 1.43) nmol/g,signif icantly lower than that in the model group(P< 0.01). CONCLUSION:Xingnaojing has a protective effect on the nerves in focal cerebra l inschemic rats,which may be related with the increased expression of antagonis t excitatory amino acid receptor.