Protection of prefrontal cortex neurons and improvement of memory in epileptic rats by 1-triacontanol cerotate

Epilepsy treatment continues to face significant challenges, including drug resistance and cognitive impairment associated with antiepileptic drugs. 1-Triacontanol cerotate (1TAC), an active component isolated from Marsilea quadrifolia Linn., has emerged as a potential therapeutic avenue for epilepsy. This study investigated the effects of 1TAC on prefrontal cortical neurons and memory retention in chronically epileptic rats, comparing its efficacy to sodium valproate. Our experiment utilized two-month-old adult male Wistar rats, randomly assigned to one of five groups: I-Vehicle Control, II-Rats receiving Pentylenetetrazol (PTZ) at a dosage of 35 mg/kg body weight intraperitoneally every 48 hours, III-Rats given 200 mg/kg body weight of sodium valproate 30 minutes prior to PTZ administration, IV and V-Rats administered 40 and 80 mg/kg body weight of 1-TAC orally 30 minutes before PTZ challenge, respectively. To assess memory performance, we conducted a passive avoidance test. Subsequently, brain specimens were processed for cresyl violet staining to assess cell densities. Results demonstrated that epileptic rats treated with sodium valproate before PTZ administration, and those given 80 mg of 1-Triacontanol cerotate exhibited significantly enhanced memory retention compared to the untreated epileptic group at both 24-and 48-hours post-challenge. Furthermore, 80 mg of 1-Triacontanol cerotate administration showed a protective effect by significantly reducing the loss of pyramidal cells in the medial prefrontal cortex. This intervention effectively minimized the loss of pyramidal neurons in the medial prefrontal cortex and mitigated memory deficits in chronically epileptic rats.