The Effects Of Tenuigenin On Expression Of NMDA Receptor And NAChRα7 In Epilepsy Model Rats

Epilepsy is a kind of brain dysfunction syndrome caused by a variety of causes.30-40% epilepsy patients are companied with different degreeof cognitive impairment.So far, the pathogenesis of cognitive impairment after epilepsy is far from being clarified.Hippocampus is an important brain area for learning and memory, and synaptic plasticity is the basis of learning and memory.NMDA receptors are closely related to synaptic plasticity, and play a crucial role in the formation of long-term potentiation.The ability of learning and memory is also closely related to the cholinergic system.Studies have indicated that acetylcholine has a promoting effect on learning and memory ability.nAChRα7 is an important subtype of nicotinic acetylcholine receptor.Tenuigenin is one of the effective constituents of Polygala Anshen Yizhi drugs.Previous studies have indicated that Tenuigenin can improve cognitive function in patients with epilepsy, but the mechanism is not entirely clear.This study intends to further explore its molecular mechanism, to add some theoretical basis for tenuigenin in improving cognitive function after epilepsy.ObjectiveTo investigate the underlying mechanisms of Tenuigenin in relieving secondary cognitive disorderby observing the effects of Tenuigenin(TEN)on expression of NMDA receptor andnAChRα7 in epilepsy model rats.Methods40 male Wistar rats were randomly divided into four groups:control group, epilepsy model group, low-dose TEN treatment group and high-dose TEN treatment group, 10 rats in each group. Epileptic model rats were made by taking intraperitonealinjection of PTZ solution. The low-dose TEN treatment group and high-dose TEN treatment group were administered with different concentrations of TEN solution at the same time ofintraperitoneal injection of PTZ solution. The control group were injected with normal saline respectively. The expression of NMDA receptors and nAChRα7 in the hippocampus CA1 area was measured by immunohistochemistry method.Then SPSS software was used for statistical analysis.Results1. Compared with the control group,the average gray-scale values of hippocampus CA1 area NMDA receptors and nAChRα7 in the model group were increased significantly(P<0.05),suggesting the expression of NMDA receptor and nAChRα7 in the model group was significantly reduced.2. Compared with the model group, the average gray-scale values of hippocampus CA1 area NMDA receptors and nAChRα7 in the low-dose TEN treatment group and high-dose TEN treatment group were decreased significantly(P<0.05), suggestin the expression of NMDA receptor and nAChRα7 in the low-dose TEN treatment group and high-dose TEN treatment group were significantly increased3. Compared with the low-dose TEN treatment group, the average gray-scale valuesof hippocampus CA1 area NMDA receptors and nAChRα7 in the high-dose TEN treatment group was decreased significantly(P<0.05), suggesting the expression of NMDA receptor and nAChRα7 in the high-dose TEN treatment group was significantly increased.Conclusion1. Compared with the control group,the expression of hippocampus CA1 area NMDA receptor and nAChRα7 in the model group was significantly reduced,which may be part of the mechanism of cognitive impairment in the epilepsy model rats.2.TEN candose-dependenting increase the expressions of hippocampus CA1 area NMDA receptor and nAChRα7 in the epilepsy model rats, which may partly explain the beneficial effects of TEN on cognitive function.