Neuroprotective Role of S-Allyl-L-Cysteine in Pentylenetetrazol-induced Epileptic Seizure in a Rat Model

Abstract

Epilepsy is a chronic non-communicable brain disease affecting approximately 50 million people of all ages worldwide. Antiepileptic drugs (AEDs) are used to manage epileptic seizures. However, AEDs may fail to control seizure activity in some patients and may cause unwanted effects of varying severity, including impairment of central nervous system (CNS) functions. Oxidative stress and imbalances between the excitatory and inhibitory neurotransmitters glutamate and GABA have been implicated in epileptic seizures, highlighting the need for acceptable treatments with fewer adverse effects. S-allyl-L-cysteine (SAC), a natural antioxidant compound, may help prevent epileptic seizures at lower cost and with fewer adverse effects. This study investigated the neuroprotective role of SAC in pentylenetetrazol (PTZ)-induced epileptic seizures in rats. Sixty male Wistar rats were divided into six groups of 10 animals each. Four groups were pretreated with SAC at 100, 200, or 400 mg/kg or with valproic acid (VPA) at 150 mg/kg before PTZ administration. Hippocampal tissues were harvested, homogenised, and centrifuged, and the supernatants were assayed for MDA, SOD, CAT, GSH, glutamate, and GABA. SAC reduced MDA and increased SOD, CAT, and GSH, indicating attenuation of oxidative stress and enhancement of antioxidant defence. Reduced glutamate and increased GABA concentrations suggest improved neurochemical balance and reduced neuronal hyperexcitability. These combined effects support the neuroprotective action of SAC in PTZ-induced seizures and its potential to limit seizure-associated oxidative and excitotoxic brain damage.