Leonurine Attenuates Neuroinflammation and Oxidative Stress in a Pentylenetetrazole-induced Epilepsy in Rats

Background Epilepsy is a complex neurological condition characterized by recurrent seizures due to abnormal neuronal activity. Objectives The major aim of this study is to examine the therapeutic activities of leonurine in a pentylenetetrazole (PTZ)-challenged epileptic seizure model in rats. Materials and Methods Epilepsy was initiated in the rats by administering 45 mg/kg of PTZ. Rats received pretreatment of leonurine (10 mg/kg) and the standard drug diazepam 30 min before the PTZ treatment. Seizure severity was evaluated in both the control and experimental rats. The levels of oxidative stress indicators, inflammatory cytokines, ion transports, and neurotransmitters were assessed utilizing the appropriate test kits. Molecular markers such as cytochrome- c (cyt- c ), caspase-3, cyclooxygenase-2 (COX-2), toll-like receptor 4 (TLR-4), mammalian target of rapamycin (mTOR), and nuclear factor kappa B (NF-κB) concentrations were studied using respective kits. Histological studies were conducted on the brain tissues of the experimental rats. Results Leonurine treatment significantly diminished seizure severity and increased locomotor activity in the epileptic rats. Leonurine treatment also effectively regulated neurotransmitters and ion transport mechanisms, reduced oxidative stress, decreased TLR-4 and high mobility group box 1 (HMGB1), decreased inflammatory cytokine, regulated protein kinase B (AKT)/mTOR axis, and diminished caspase-3, cyt- c , COX-2, and NF-κB concentrations in both cortex and hippocampal regions of the rats with epilepsy. The findings of histopathological studies also proved the therapeutic effects of leonurine. Conclusion It may be concluded that leonurine offers a promising therapeutic candidate to treat epilepsy. Further studies are necessary to understand the underlying mechanisms of leonurine’s therapeutic benefits on epilepsy.