Abstract

Alcohol consumption has been found to be associated with gastric ulcers, including gastric mucosal lesions. Salusin-α and salusin-β are bioactive peptides having 28 and 20 amino acids, respectively. Salusin-α and salusin-β immunoreactivity has been detected in the stomach and in the intestines. It has been reported that the salusins regulate the cytokine levels and decrease the infarct area in the heart tissue after ischemia. In this study, we investigated the effects of the salusins in the gastric injury formed with ethanol. Thirty-two sprague Dawley male rats were randomly divided into four groups, including eight rats in each group as follows: Group 1: control; Group 2: ethanol 5 mL/kg; Group 3: ethanol 5 mL/kg+5 nmol/kg salusin-α; Group 4: ethanol 5 mL/kg+5 nmol/kg salusin-β. The salusin-α level increased at a significant level in the ulcer group formed with ethanol (p<0.001); the change in the salusin-β level is not significant. As for malondialdehyde (p<0.05) and myeloperoxidase (p<0.001), when compared with the control group, tumor necrosis factor-α (p<0.05) levels increased in the group to which ethanol was applied and decreased significantly with the application of salusins. Levels of GSH and IL-1β did not change at a significant level. In addition, histopathologic analysis demonstrated that, in salusin-administered groups, mucosal injury and caspase-3 expressions were reduced. The suppression of salusin-α and salusin-β on caspase-3 expression by means of their effects on oxidative injury and TNF-α levels shows that these two hormones could serve as anti-ulcerative agents.

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