The results suggest that an increase in the vasoconstrictive ET-1 level combined with a decrease in regulatory cytokine, IL-4, and a loss of compensatory action by cNOS may be responsible for the gastric mucosal injury caused by indomethacin. Our findings also indicate the value of sucralfate in countering the untoward gastrointestinal side effects of nonsteroidal anti-inflammatory drug therapy.

Gastric mucosal inflammatory responses to H. pylori lipopolysaccharide are characterized by a massive enhancement of the proinflammatory cytokine TNF-alpha and epithelial cell apoptosis and repression of IL-4. Our data also show that sucralfate is capable of inducing expression of the regulatory cytokine IL-4 and the suppression of apoptotic events triggered in gastric mucosa by the increase in TNF-alpha that is elicited by H. pylori lipopolysaccharide.