Protective Effects of Allantoin on Neural Cells of Hippocampal Region and Cognitive Function in a Mouse Model of Temporal Lobe Epilepsy

Objective: Excitotoxic damage results in cell death in several human neurodegenerative diseases. Epilepsy is one of the most common neurological disorders and it causes complications. To this end, we examined the protective role of allantoin (AL) in a model of excitotoxic neuronal death induced by intraperitoneal injection of kainic acid (KA) in mice. Methods: Two-month-old C57 male mice (n=35) were divided into five groups: control (received 0.9% saline), AL (received 10 mg/kg of AL), KA (received a single dose of 10 mg/kg of KA), KA+AL10 and KA+AL15 groups (received a single dose of 10 mg/kg of KA then were treated with 10 mg/kg of AL or 15 mg/kg respectively). On the 14th day of the experiment, learning and memory were tested using a shuttle-box. The number of intact neurons and damaged neural cells in hippocampal CA1 and CA3 were assessed by Nissl staining and Flour-J B immunohistochemistry, respectively. Results: The results showed that injection of KA decreased the latency time while administration of 10 mg/kg AL improved memory. In addition, there was a significant difference between KA and KA+AL10 mg/kg groups (p<0.01). The histological results revealed that the use of 10 mg/kg AL significantly increased the number of intact pyramidal cells in the hippocampal CA1 and CA3 regions compared with the KA group (p<0.01). Moreover, neurodegeneration of the hippocampal region was significantly decreased in the groups treated with AL compared with the KA group (p<0.05). Conclusion: This study indicated that AL at a concentration of 10 mg/kg/day improved neurodegenerative complications following temporal lobe epilepsy.