Lansoprazole is a proton-pump inhibitor (PPI) which prevents the stomach from producing gastric acid.
Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.
DMSO ：74 mg/mL (200.35 mM)
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. 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.
Lansoprazole inhibits acute inflammatory reactions as well as intestinal mucosal injuries induced by ischemia-reperfusion or indomethacin administration in rats. Lansoprazole significantly inhibits intestinal injuries induced by ischemia-reperfusion or indomethacin. lansoprazole administered exogenously prevents the small intestine against ischemia-reperfusion or indomethacin-induced damage, the action being dependent on its anti-inflammatory and anti-oxidative responses.
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