Helicobacter pylori eradication to prevent gastric cancer: Underlying molecular and cellular mechanisms

Figure 1 Expression of COX-2, nitrotyrosine and Ki-67 immunoreactivity in human gastric mucosa with intestinal metaplasia after cure of the H pylori infection. A: COX-2 immunostaining; B: nitrotyrosine immunostaining; C: Ki-67 immunostaining. The overexpression of COX-2 and nitrotyrosine, adduct of nitric oxide, are reported in gastric mucosa with H pylori infection[66,68,70,71]. In these photographs, metaplastic gland with goblet cells (in the left side of each photograph) and non-metaplastic gastric glands (in the right side) are shown. COX-2 and nitrotyrosine immunoreactivities continue to exist in gastric mucosa with intestinal metaplasia after the successful H pylori eradication with PPI-triple therapy.