Ghrelin improves pilocarpine‑induced cerebral cortex inflammation in epileptic rats by inhibiting NF‑κB and TNF‑α.

Ghrelin has a protective function in the nervous system, including anti‑inflammatory and antiapoptotic. The objective of the present study was to examine the anti‑inflammatory effects of the ghrelin on nuclear factor‑κB (NF‑κB) and tumor necrosis factor‑α (TNF‑α) gene and protein expression in an epileptic seizure model. Epileptic seizures were induced in healthy male Wistar rats (~3 weeks old) with 300 mg/kg pilocarpine, and brains from rats with Racine stage IV or V seizures were investigated further in the present study. The effect of ghrelin treatment on TNF‑α and NF‑κB protein and mRNA expression was assessed by immunohistochemistry and semi‑quantitative reverse transcription polymerase chain reaction, respectively. TNF‑α and NF‑κB protein and mRNA expression were significantly increased in the pilocarpine and the pilocarpine + saline groups compared with the control group. Ghrelin intervention significantly decreased TNF‑α and NF‑κB protein and mRNA expression compared with the pilocarpine and the pilocarpine + saline groups, although it did not reduce expression levels to those seen in the normal control group. Ghrelin reduces inflammation in cortical neurons following epileptic seizure, and therefore may reduce necrosis and the loss of nerve cells, preserving the normal function of the cortex. Ghrelin may alleviate cortex inflammation reaction by adjusting the TNF‑α and NF‑κB so as to reduce child epilepsy attack repeatedly. The findings of the present study may contribute to the clarification of the role of Ghrelin in the brain in seizure‑induced immune system physiology and may also present novel approaches to the etiology and treatment of epileptic seizures.