Potencjalnie ochronne dla mózgu i przeciwpadaczkowe właściwości ekstraktu etanolowego oraz jego wpływ na zaburzenia nastroju towarzyszące modelowi epilepsji indukowanej pentylentetrazołem: badania behawioralne, biochemiczne i histologiczne

Epilepsy is a chronic neurological disorder that is strongly influenced by oxidative stress and neuronal death, two major pathophysiological factors. According to various recent studies, extract (GLE) may have antioxidant properties. However, there is little evidence to support its effectiveness in treating epilepsy. Here, we examined the neuroprotective qualities of GLE (300 mg/kg) against seizures induced by pentylenetetrazol (35 mg/kg). Four groups of eight male Wistar rats per group were randomly assigned: control, Pentylenetetrazol (PTZ), GLE-300 and Diazepam. The animals received an intraperitoneal dose of PTZ (35 mg/kg) every 48 h (11 injections in total) for 21 days to create an epilepsy model. The Racine five-point score was used to assess seizure severity. Anxious behavior, locomotor and exploratory activity were assessed using the open field test (OFT) and the elevated plus maze test (EPM), while the forced swim test (FST) was used to assess depressive behavior. Markers of oxidative stress, including malondialdehyde (MDA), nitric oxide (NO), and the enzymatic activities of superoxide dismutase (SOD) and catalase, were measured using the 2-thiobarbituric acid method (TBA), Griess reagent, nitro blue tetrazolium (NBT) reduction, and hydrogen peroxide decomposition. We performed a histological study of the prefrontal cortex (PFC) to quantify neuronal loss in the cortical layers using Nissl staining. All in all, our results showed that GLE reduces the severity of convulsive seizures during the induction of epilepsy ( < 0.001) and alleviates anxious ( = 0.005) and depressive ( = 0.008) behaviors while reducing neuronal damage. As well as significantly reduce NO and MDA levels ( < 0.001), and restore catalase ( = 0.005) and SOD ( = 0.010) enzyme activities in biochemical evaluation. Histologically, the GLE reduces neurodegeneration in the PFC due to its antioxidant and neuroprotective properties ( = 0.003). In conclusion, the experimental results indicate that GLE significantly attenuates the behavioral, biochemical, and histological alterations induced by PTZ, thus supporting its neurotherapeutic potential in the PTZ-Kindling model of epilepsy.