Edaravone acts as a potential therapeutic drug against pentylenetetrazole-induced epilepsy in male albino rats by downregulating cyclooxygenase-II.

introductionThe effects of edaravone against pentylenetetrazole (PTZ)-induced epilepsy in male albino rats were investigated. Edaravone is a well-known commercial drug used in the treatment of strokes and amyotrophic lateral sclerosis (ALS). Antioxidant and free radical scavenging activities of edaravone have been reported in patients with ALS.

methodsIn this study, the experimental groups were as follows: sham, control, 5 mg/kg edaravone, and 10 mg/kg edaravone. Behavioral assessment, determination of biochemical markers, apoptosis, nitric oxide (NO), and mRNA and protein expression of cyclooxygenase-II (COX-II) were carried out. Seizure incidence, including generalized tonic-clonic seizure (GTCS) and minimal clonic seizure (MCS), was directly associated with PTZ administration in rats.

resultsEdaravone supplementation substantially increased MCS and GTCS latency in rats, and biochemical markers were significantly altered in the brain tissue of PTZ-treated rats. Edaravone treatment normalized altered biochemical markers compared with the untreated control. Apoptosis and NO levels were significantly reduced by more than 50% compared to their respective controls. COX-II mRNA was increased by 130% in PTZ-treated rats, while edaravone supplementation reduced mRNA and protein expression of COX-II by more than 20% and 40%, respectively. Immunohistochemistry indicated that COX-II protein expression was reduced by 13.2% and 33.7% following supplementation with 5 and 10 mg/kg edaravone, respectively.

conclusionTaken together, our results suggest that edaravone functions by downregulating the levels of COX-II and NO and is a potential candidate for the treatment of PTZ-induced epilepsy.