Melissa officinalis L. ameliorates oxidative stress and inflammation and upregulates Nrf2/HO-1 signaling in the hippocampus of pilocarpine-induced rats.

Epilepsy is characterized by recurrent epileptic seizures, and its effective management continues to be a therapeutic challenge. Oxidative stress and local inflammatory response accompany the status epilepticus (SE). This study evaluated the effect of Melissa officinalis extract (MOE) on oxidative stress, inflammation, and neurotransmitters in the hippocampus of pilocarpine (PILO)-administered rats, pointing to the involvement of Nrf2/HO-1 signaling. Rats received PILO via intraperitoneal administration and were treated with MOE for 2 weeks. MOE prevented neuronal loss; decreased lipid peroxidation, Cox-2, PGE2, and BDNF; and downregulated glial fibrillary acidic protein in the hippocampus of PILO-treated rats. In addition, MOE enhanced GSH and antioxidant enzymes, upregulated Nrf2 and HO-1 mRNA abundance, and increased the nuclear translocation of Nrf2 in the hippocampus of epileptic rats. Na/K-ATPase activity and GABA were increased, and glutamate and acetylcholine were decreased in the hippocampus of epileptic rats treated with MOE. In conclusion, MOE attenuated neuronal loss, oxidative stress, and inflammation; activated Nrf2/HO-1 signaling; and modulated neurotransmitters, GFAP, and Na/K-ATPase in the hippocampus of epileptic rats. These findings suggest that M. officinalis can mitigate epileptogenesis, pending further studies to explore the exact underlying mechanisms.