LansoprazoleS1354

Lansoprazole inhibits gastric acid secretion via inhibition of gastric hydrogen/potassium adenosine triphosphatase (H+,K(+)-ATPase), an enzyme of the gastric parietal cell membrane that forms part of the proton pump that performs the final step in the acid secretory process. Lansoprazole binds covalently to parietal cell H+,K(+)-ATPase, rendering it nonfunctional and inhibiting the secretion of gastric acid. ^[1] Lansoprazole is a strong anti-secretory agent that acts on gastric H+/K+-adenosine triphosphatase (H+/K+ ATPase) of parietal cells. Lansoprazole inhibits the increased expression of vascular adhesion molecules, the activation of neutrophils, and the production of pro-inflammatory cytokines from activated endothelial cells. Lansoprazole induces several genes, including phase II detoxifying enzyme (NADPH-ubiquinone oxidoreductase, glutathione S-transferase) and antioxidant stress proteins (HO-1, thioredoxin reductase, and superoxide dismutase) in gastric epithelial cells. Lansoprazole significantly inhibits the production of CINC-1 from stimulated RGM-1 cells with IL-1β. Lansoprazole up-regulates HO-1 expression throughout Nrf2 in rat gastric epithelial cells, and the up-regulated HO-1 has anti-inflammatory effects. ^[2]