Obestatin Protective Role Againest Stress Gastric Ulcer in Rat, ABEER A. KHALEFA
Abstract
Background: Acute hemorrhagic and erosive gastropathy may represent a potentially life-threatening condition. Obestatin hormone has been recognized as a key factor in regulating appetite and energy homeostasis. Obestatin is produced in the stomach, but little is known about his influence on gastric mucosal integrity.
Aim of Work: This study was designed to elucidate the effect of Intra-peritoneal "IP" administration of obestatin on acute gastric ulcer induced by 6 hours immobilization stress in rats, with or without suppression of nitric oxide "NO" by NG-Nitro-L-arginine methyl ester (L-NAME) in a trial to explore the possible involved mechanisms of action.
Material and Methods: The study had been carried out on 40 adult male albino rats. The animals were divided into three main groups: Group I (control group) (n=8), group II obestatin treated group "10, 30,100μg/Kg. BW, IP (n=8 for each dose). Group III treated with L-NAME (10μg/Kg. BW "Sc") 15 minutes before obestatin administration (30μg/Kg. BW "IP"). In all studied groups ulcer score, ulcer index and preventive index were evaluated, in addition, gastric superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) activities were measured.
Results: IP administration of obestatin in a dose dependent manner, resulted in a significant decrease in ulcer score (p<0.001) and ulcer index with increase in preventive index together with increase activities of gastric SOD (p<0.001), CAT (p<0.001) and GPX activities (p<0.01, p<0.001 and p<0.001 with respect to the obestatin dose). In L-NAME pretreated animals, the ulcer prevention ability of obestatin was significantly reduced when compared to that of the same dose of obstatin in group II (30μg/Kg. BW) (p<0.001). How-ever, there was still significant reduction in ulcer score and ulcer index when compared with that of the control group (p<0.001).
Conclusions: This study revealed that, potent dose depen-dent protective effect of exogenous obestatin against stress-induced gastric lesions accompanied by a significant increase in gastric antioxidant enzymatic activity. In addition, endog-enous NO release is involved in the mechanism of obestatin action as pretreatment with L-NAME partially attenuated this protective effect indicating that nitric oxide release is not the