Nesfatin‑1 exerts anticonvulsant effect by reducing oxidative stress in experimental epilepsy model.

Abstract

Neuropeptides play an important role in the pathogenesis of epilepsy. In the present study, the effect of nesfatin‑1, a neuropeptide, was investigated on penicillin‑induced epilepsy model. Epileptiform activity was induced by an injection of penicillin into the somatomotor cortex at 56 albino Wistar rats. Nesfatin‑1 (i.c.v.) was administered at five different doses (12.5, 25, 50, 100, and 200 pmol) 30 min after a penicillin administration. Astressin 2B, a corticotropin‑releasing factor (CRF) receptor antagonist, was administered 10 minutes later the effective dose of nesfatin‑1 (50 pmol, i.c.v.). Superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR) and malondialdehyde (MDA) levels in cerebrum were analysed by ELISA method. Nesfatin‑1, at the doses of 25, 50 and 100 pmol, significantly reduced the frequency of epileptiform activity. However, none of the doses of nesfatin‑1 had any effect on the amplitude of epileptiform activity. Astressin 2B alone did not show any effect on epileptiform activity. In addition, astressin 2B had no effect on the anticonvulsant effect of nesfatin‑1. Nesfatin‑1 (at the doses of 25, 50, 100 pmol) did not alter SOD and GSH levels, but significantly increased the GPx and GR levels. Nesfatin‑1 (at a dose of 50 pmol) significantly decreased the MDA level in the cerebrum. Nesfatin‑1 shows anticonvulsant effect and astressin 2B did not affect the anticonvulsant effect of nesfatin‑1. We suggest that nesfatin‑1 has oxidative stress‑mediated anticonvulsant effect in the penicillin‑induced epileptic activity.