Background: Seizures and associated oxidative stress are hallmark features of epilepsy and other neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and traumatic brain injury. These conditions share common pathophysiological mechanisms including excitotoxicity, mitochondrial dysfunction, and redox imbalance that contribute to neuronal damage and disease progression. Targeting oxidative stress pathways has emerged as a promising translational strategy for neuroprotection and seizure control. This study aims to evaluate the effects of wogonin, a flavonoid compound, on seizure latency and oxidative brain damage induced by pentylenetetrazol (PTZ) in a mouse model. Methods: Adult male mice (25–30 g) were randomly assigned to control and experimental groups (n=10 per group). Seizures were induced via intraperitoneal injection of PTZ (100 mg/kg). Experimental groups received wogonin (1, 5, or 10 mg/kg, i.p.) 30 minutes prior to PTZ administration. Seizure latency was recorded. Post-seizure, mice were euthanized, and hippocampal and cortical tissues were harvested for biochemical analysis of oxidative stress markers, including nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and total thiol content. Results: PTZ administration significantly decreased the latency to both minimal clonic seizures (MCS) and generalized tonic-clonic seizures (GTCS). Wogonin pretreatment significantly increased MCS and GTCS latencies in a dose-dependent manner. Oxidative stress markers NO and MDA were significantly elevated following PTZ administration, and wogonin pretreatment at doses of 5 and 10 mg/kg significantly reduced their levels. SOD and CAT activities were significantly restored in groups treated with 5 and 10 mg/kg of wogonin, while total thiol content was notably increased at the highest dose. Conclusion: These findings suggest that wogonin may serve as a potential therapeutic agent for managing seizure disorders and oxidative stress-related neurological damage, although further studies including pharmacokinetic profiling and validation in human models are needed to confirm its clinical relevance.
Bibak et al. (Mon,) studied this question.