Abnormal neuronal damage and inflammation in the hippocampus of kainic acid‐induced epilepsy mice

In this study, we established a mouse model of epilepsy and analysed abnormal neuronal damage and inflammation in the hippocampus of mice with kainic acid (KA)‐induced epilepsy to provide the basis for the pathogenesis of epilepsy. C57 mice, aged 4 weeks, were injected intraperitoneally in the KA group with 20 mg/kg of KA and in the sham experimental group with normal saline. The whole brain and hippocampus of mice in the sham experimental group and KA epilepsy model group were collected on days 7, 14, 21 and 28 after injection. The difference in the protein expression in the hippocampus was detected using fluorescence immunohistochemistry. The hippocampal tissue was also collected and frozen to detect protein expression by western blot. The results of the haematoxylin and eosin (HE) and Nissl staining showed that the mouse model of temporal lobe epilepsy could be established by intraperitoneal injection of KA, and the success rate of the model was 53.8%. The expression of DCX‐, β‐catenin‐, GFAP‐ and Iba‐1‐labelled glial cells in the KA‐induced epilepsy model group were higher than those in the sham group. The results of western blotting showed that the expression of DCX and β‐catenin in the KA‐induced epilepsy model group was higher than that in the sham experimental group, while the expression of N‐cadherin and Iba‐1 on days 14 and 28 was significantly ( P < .05) higher than that in the sham experimental group. In KA‐induced epilepsy model group, the expression of Bcl‐2 was decreased, while the expression of Bad and PUMA was increased.