IL1B and ulcer disease: These effects occur through the inhibition of the cyclooxygenase (COX) enzymes, resulting in a marked decrease in the levels of prostaglandins [41], but the reactive-oxygen-species (ROS)-induced enhancement in lipid peroxidation plays an important role in the mechanism of gastric damage induced and the increase in free radical metabolites depends possibly upon neutrophil activation and is associated with the significant increase in lipid peroxidation, the fall in the gastric blood flow at ulcer margin, and the excessive release of the proinflammatory cytokine such as IL-1b [40].