Objective: 

Ghrelin, a peptide released from stomach with potent effects on appetite, also mediates behavioral responses to stress. The aim was to investigate the effect of ghrelin on stress-induced oxidative injury.

Methods: 

Female Sprague-Dawley rats were exposed to an acute psychological 30-min water avoidance stress (WAS). Ten minutes before WAS, either glucocorticoid-receptor antagonist (RU-486, 10 mg/kg, ip) or oxytocin-receptor antagonist (atosiban, 1 mg/kg, ip) was injected, and 5 min later rats were injected with either ghrelin (10 ng/kg) or saline. After cessation of WAS, rats were decapitated to obtain gastric and colonic samples for the measurement of lipid peroxidation (LP), gluthatione (GSH) levels, myeloperoxidase (MPO) activity, and for histological analysis. For statistical analysis Student's t test or ANOVA was used.

Results: 

Compared to control group, LP levels and MPO activities were increased in both tissues of saline-treated stress group (p<0.05–0.001), which were reversed in the ghrelin-treated stress group (p<0.05–0.001). Colonic and gastric LP and MPO activities were increased in atosiban pre-treated groups as compared to ghrelin-injected stress group (p<0.05–0.001). Gastric GSH levels, which were depleted in stressed and atosiban-pre-treated groups, were replenished in ghrelin-injected stress group (p<0.05). Histological analysis verified stress-induced damage in both tissues with significant reductions in damage scores of ghrelin-treated stress group and exaggerated damage in atosiban- and RU-486-treated stress groups.

Conclusions: 

Ghrelin ameliorated stress-induced gastric and colonic oxidant damage, which was worsened by blocking oxytocin receptors. Thus, it appears that the protective effect of ghrelin against stress-induced oxidative damage involves the activation of oxytocin receptors.