A Low Dose of Edaravone Decreases the Epileptiform Activity in the Absence Epilepsy Model by Reducing Oxidative Stress and Neuroinflammation

Edaravone is a potent anti-inflammatory and antioxidant agent used in amyotrophic lateral sclerosis treatment. The effect of Edaravone on absence epilepsy was investigated in WAG/Rij (Wistar Albino Glaxo from Rijswijk) rats, a genetic animals model of absence epilepsy. Twenty-eight WAG/Rij rats were randomly assigned to four groups: control, and Edaravone-treated groups receiving 1, 10, or 30 mg/kg. A tripolar electrode was inserted into the skull using the stereotaxic device for electrocorticography (ECoG) recording. Then, the animals were allowed to recover. Baseline ECoG recordings were obtained from all groups, and then Edaravone was administered at the indicated doses for 21 days. ECoG records of all groups were retaken on the 22nd day. The brain was dissected and sent for biochemical analysis at the end of the experiment. Total antioxidant status (TAS), total oxidant status (TOS), and tumor necrosis factor-alpha (TNF-α) levels in brain tissue were measured using enzyme-linked immunosorbent assay (ELISA). The administration of 1 and 10 mg/kg Edaravone decreased the number and duration of spike-wave discharges (SWDs), but 30 mg/kg Edaravone increased the number and duration of SWDs. All Edaravone doses did not change the amplitude. In the biochemical analysis, 1 and 10 mg/kg Edaravone increased TAS level and decreased TOS and TNF-α levels compared to control group. 30 mg/kg Edaravone did not affect TAS, TOS, and TNF-α levels compared to control group. The present study exhibited that low doses of Edaravone for long-term treatment reduced the incidence of SWDs in WAG/Rij rats by reducing oxidative stress and neuroinflammation. The high doses of Edaravone increased SWDs incidence in the same model.