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Abstract

The protective effects of the proton pump inhibitor lansoprazole on gastric mucosal damage induced by ethanol-HCl or hemorrhagic shock were investigated in the present study. The morphometric analysis of gastric histological sections revealed that lansoprazole dose-dependently reduced mucosal injury evoked by ethanol-HCl (ED50 = 24.3 micromol/kg) or hemorrhagic shock (ED50 = 38.9 micromol/kg), these effects being associated with marked increments of Alcian blue recovery from gastric bound mucus (ED50 = 31.4 micromol/kg and 27.6 micromol/kg, respectively). In addition, lansoprazole inhibited gastric acid secretion from pylorus-ligated rats (ED50 = 9.8 micromol/kg). Further experiments, performed on rats with ethanol-HCl-induced gastric injury, indicated that the protective effects of lansoprazole were not modified by L-365,260, suramin, N(G)-nitro-L-arginine, or systemic ablation of capsaicin-sensitive sensory nerves, whereas they were partly blocked by indomethacin and fully prevented by N-ethyl-maleimide. In addition, lansoprazole did not modify somatostatin concentrations in gastric mucosa. The present results provide evidence that lansoprazole prevents the necrotic damage of gastric mucosa induced by ethanol-HCl or hemorrhagic shock. According to the rank order of ED50 values, these effects appear to depend mainly on the enhancement of the gastric mucus barrier rather than on the reduction of acid secretion. It is also proposed that an increased production of prostaglandins, as well as an increased availability of sulfhydryl compounds at level of gastric mucosa may account for the gastroprotective effects of lansoprazole.

Comparative study of proton pump inhibitors on dexamethasone plus pylorus ligation induced ulcer model in rats

“…This inhibition potentiates the inhibitory effect on the proton pump[23]. Similarly lansoprazole exerts its gastroprotective effects by increased bio-availability of mucosal sulfhydryl compounds and possibly prostaglandins[24]. …”

Benzimidazole covalent probes and the gastric H+/K+-ATPase as a model system for protein labeling in a copper-free setting

“…It is thought to play a role in both immune defense and epithelial differentiation 38 and has also been reported to bind Helicobacter pylori 39 . Interestingly, Benzimidazole compounds are commonly used to treat H.pylori infection 40 with an unknown cellular target and both DMBT1 and benzimidazole compounds have been reported to play a protective role for gastrointestinal mucosa 41, 42 . It would be interesting to carry out more studies to examine the physiological interaction between DMBT1 and benzimidazole compounds.…”

Petroselinum Crispum is Effective in Reducing Stress-Induced Gastric Oxidative Damage

“…In the present study, we also found a significantly reduced HDS in the stress + LPZ group compared to the stress group (p<0.05). Maiti et al ( 54 ) and Blandizzi et al ( 55 ) found LPZ effective in protecting gastric mucosa. The therapeutic effect of LPZ on gastric mucosal damage is found to be related to its mucus-increasing effect rather than its aciddecreasing effect ( 56 , 57 , 58 ).…”

“…In ulcer studies, increased MDA and SOD values, and decreased CAT, GSH and GSH-Px values or decreased MDA and SOD values, and increased CAT, GSH and GSH-Px values have been reported ( 34 , 35 , 36 , 37 , 38 , 39 , 40 , 59 , 60 ). LPZ was shown to increase sulfhydryl compounds such as GSH in particular, and thereby prevent gastric damage ( 55 , 61 ). LPZ, indeed, is known to support the antioxidant system ( 52 , 59 , 60 ).…”