Apoptosis‑antagonizing transcription factor is involved in rat post‑traumatic epilepsy pathogenesis

Abstract

The present study aimed to explore the pathogenesis behind post‑traumatic epilepsy (PTE). In the present study, a chloride ferric injection‑induced rat PTE model was established. The expression levels of apoptosis‑antagonizing transcription factor (AATF), cleaved caspase‑3, p53, Bcl‑2 and Bax were measured by western blotting or immunofluorescence staining (IF). The expression of AATF <em>in vivo</em> was downregulated by microinjection of lentiviral‑mediated short‑hairpin RNA. Compared with control and sham groups, at day 5 after PTE, neuron apoptosis was significantly increased and the expression levels of AATF, p53, cleaved caspase‑3 and Bax were significantly upregulated. In addition, IF revealed co‑localization of AATF and cleaved caspase‑3 in the cortex. Additionally, AATF was expressed mainly in neurons and astrocytes. Following AATF inhibition, the expression levels of p53 and cleaved caspase‑3 were significantly reduced as compared with the control group. Taken together, these findings suggested that following PTE, AATF is involved in neuronal apoptosis and may serve as a potential target for its alleviation.