The Relation Between Memory And Expression Of NMDA Subunite Of Hippocampal In Rat With Brain Ischemical Reperfusion And Intervention Of Ginsenoside Rg₂

Objective To use an ischemical reperfusion injury rat model by pulsinelli-4-VO andobserve the changes of the expression of Glu, N-methy-D-asparagic acid (NMDA)receptor subunits NR₁ and NR_2B and ability of learning and memory after procerebrum(hippocampus) ischemic reperfusion injury, and approach the pathogenesy of learning andmemory disorder induced by ischemic reperfusion injury, and the intervention ofginsenoside Rg₂ on the learning and memory disorder after procerebrum (hippocampus)ischemic reperfusion injury.Methods Pulsinelli-4-vessel occlusion was performed on rat (n=56) to make awhole brain ischemic reperfusion injury model. Ginsenoside Rg₂ in high dose (10.0mg/kgBW), moderate(5.0mg/kg) and low dosages(2.5mg/kg) were given respectively to the ratsin experimental groups(n=8 in each group). Morris water maze was used to detect theability of learning and memory, immunohistochemistry and image analysis wereperformed to study the expression of Glu, NR₁ and NR_2B of the hippocampus neuron fromdifferent groups.Results The releasing of Glu and the expression of NR₁ and NR_2B of hippocampusneutrons in the model rats were more obviously than that of sham-operation rats afterprocerebrum (hippocampus) ischemic reperfusion injury, and howere the expression of NR₁and NR_2B were significantly reduced, and escaping eclipse period was significantlyshorten in the animals in high dose and moderate dose ginsenoside Rg₂ groups,thedifference has significance (P＜0.01) compared with model group.Conclusions The massive release of glutamate activated excessively the NMDAreceptors after cerebral ischemic reperfusion injury. The expressions of NMDA receptorsubunits NR₁ and NR_2B were increased, which induced the function of the receptors werechanged and resulted in the [Ca²⁺]i overloading in the intra-cellular, that mediate a seriesof Ca²⁺-depending biochemical events in the intra-cellular and the injury of the neurons,therefore ability of learning and memory were lowed. Ginsenoside Rg₂ can interfere in theexpression of excitatory amino acid receptors subunits by inhibiting the release ofglutamate, and influence fuctional change of the receptors, thereby play a protective role onlearning and memory after cerebral ischemic reperfusion injury.