The antioxidant and anticonvulsant effects of ellagic acid in kainic acid-induced temporal lobe epilepsy in mice.

Oxidative stress (OS) resulting from high levels of free radicals contributes to the initiation and progression of epilepsy. Temporal lobe epilepsy (TLE) is associated with alteration in the structure and function of the hippocampus and is modeled in mice using kainic acid (KA). In this study, the neuroprotective effect of ellagic acid (EA) on KA-induced epilepsy in mice was evaluated. Sixty male Swiss albino mice were assigned to six groups: I received normal saline (NS; 10 ml/kg, intraperitoneally (i.p.)); II, received KA (15 mg/kg, i.p.); III, received diazepam (20 mg/kg, i.p.) and KA (15 mg/kg, i.p.); IV-VI, received EA (10, 20 and 40 mg/kg, i.p.), and KA (15 mg/kg, i.p.). Treatments were done 30 min before KA injection. Seizure (latency, duration, activity) and mortality were monitored for 2 h post-injection. OS was evaluated by measuring MDA, NO, and GSH levels and CAT, SOD, and GPx activities. Levels of TNF-α in the brain tissue were measured. Furthermore, a histological examination of the hippocampus was carried out. RESULTS: showed that EA pretreatment caused a decline in seizure activity score and duration compared to the KA-treated group. EA pretreatment reduced mortality in KA-treated mice. EA suppressed the generation of MDA and NO; whereas it preserved GSH and the activity of GPx, SOD, and CAT. Additionally, EA exerted anti-inflammatory effects by reducing TNF-α level. Histopathologically, EA reduced KA-induced neuronal damage. EA demonstrated protective effects against KA-related epilepsy and brain damage. Due to its anti-inflammatory and radical scavenging properties, EA may be considered a potential therapeutic option in epilepsy.