ObjectiveExplore the mechanism of action of Kruppel-like factor 4 (KLF4) in the oxidative damage model of hippocampal neurons in mice induced by glutamate. MethodsTo clarify the role of KLF4 and glutamate in the oxidative toxicity of epilepsy, the mouse hippocampal neuron cell line (HT22) was adopted, and a neuronal death excitotoxicity cell model was formed by induction with glutamate as the in vitro epilepsy experimental model. The expression level of KLF4 was detected by Real-Time PCR. HT22 cells were transfected with KLF4-specific siRNA, and the experiments were grouped as follows: Ctrl group, Glu group, Glu + siKLF4-1 group, and Glu + siKLF4-2 group. The cell viability of each group was detected by the CCK8 method. ResultsKLF4 was significantly increased in the epilepsy model of HT22 cells induced by glutamate, while downregulation of KLF4 improved the proliferation and viability of neurons in the epilepsy model of HT22 cells induced by glutamate. ConclusionIn the hippocampal neuron cells of epileptic mice, KLF4 is highly expressed. The downregulation of KLF4 improves the proliferation function and vitality of glutamate-induced HT22 cells, indicating that KLF4 may contribute to the occurrence and development of epilepsy by participating in the regulation of oxidative stress responses.
