Iron-induced neuronal damage in a rat model of post-traumatic stress disorder

摘要: Previous studies have shown that iron redistribution and deposition in the brain occurs some neurodegenerative diseases, oxidative damage due to abnormal level is a primary cause of neuronal death. In present study, we used single prolonged stress (SPS) model mimic post-traumatic disorder (PTSD), examined whether was involved progression PTSD. The anxiety-like behaviors SPS group were assessed by elevated plus maze (EPM) open field tests, levels measured inductively coupled plasma optical emission spectrometer (ICP-OES). Expression glucocorticoid receptors transferrin receptor 1 (TfR1) ferritin (Fn) detected Western blot immunohistochemistry selected areas; TfR1 Fn mRNA expression quantitative-polymerase chain reaction (Q-PCR). Ultrastructures hippocampus observed under transmission electron microscope. Our results showed exposure induced symptoms increased serum cortisol concentration key areas such as hippocampus, prefrontal cortex, striatum. region-specific changes both protein Fn. Moreover, swelling mitochondria cell apoptosis neurons regions with accumulation. We concluded cognition-related subsequently injury, indicating may function pathology