Post-traumatic epilepsy (PTE) is a paroxysmal functional disorder secondary to traumatic brain injury (TBI), which is a common and devastating sequela after brain trauma. At least 80% of patients develop epileptic seizures within one year following traumatic brain injury, whereas the specific mechanism underlying epileptogenesis remains unclear. After brain trauma, blood infiltrates into tissues, and erythrocytes lyse and release iron complexes that deposit in brain tissue. Studies have even demonstrated that the mere presence of blood in cortical tissue predisposes to the occurrence of epilepsy. Animal experiments have also confirmed that iron is epileptogenic and can well simulate the pathophysiological changes of post-traumatic epilepsy. Oxygen free radicals, hydroxyl radicals and hydrogen peroxide produced by iron oxidation cause oxidative stress damage, rendering neuronal cell membranes more prone to depolarization, thereby leading to epilepsy.

SD rats (male, 200–300 g)
Modeling method: FeCl₃ solution was injected at a constant rate into the sensorimotor cortex of rats. The traumatic epilepsy model was successfully established 30 days later.
Evaluation indicators: serum ELISA, HE staining

Serum ELISA

HE staining of hippocampal tissue