Ghrelin gene expression in rats with ethanol-induced gastric ulcers: a role of melatonin

The aim of the present work was to reveal the mechanisms of melatonin treatment on ethanol-induced gastric mucosal lesions in rats, including its role in the induction of ghrelin biosynthesis.

Sixty male Wistar rats were divided into 3 groups (20 in each group): a) control group, b) ulcer group (100% ethanol was given intragastrically (i.g.) in a dose of 1 ml/100 g of body weight), and 3) melatonin-treated group, which received a single dose (25 mg/kg) of melatonin (Biovea) i.g. 30 min before ulcer induction with ethanol. Reduced glutathione (GSH) and malondialdehyde (MDA) were measured in tissues and ghrelin levels determined in the serum. RNA isolation and RT-PCR expression of ghrelin were performed. Both macroscopic and microscopic examinations of gastric mucosa were done in all groups.

Significant decrease in ghrelin levels and mRNA expression and reduced levels of GSH were observed in ulcer group of rats in comparison with controls. All parameters studied were significantly increased after treatment with melatonin in comparison with ulcer bearing group of rats. On the other hand, the tissue levels of MDA were significantly increased in ulcer group of rats in comparison with controls and significantly decreased after melatonin treatment in comparison with the ulcer group of rats. Histological examinations revealed severe mucosal lesions induced by ethanol which were significantly improved by melatonin administration.

The present data indicate that melatonin may have a potential impact in the treatment of peptic ulcer not only via its known antioxidant effect but also via induction of the ghrelin biosynthesis, as it was documented by significant increase in ghrelin mRNA expression.