Maróstica Marta, Arçari Demetrius Paiva, Bartchewsky Waldemar, Trevisan Miriam, Ribeiro Marcelo Lima, Pedrazzoli José, Hoehr Nelci Fenalti, Gambero Alessandra
Clinical Pharmacology and Gastroenterology Unit, São Francisco University Medical School, Bragança Paulista, SP, Brazil.
Scand J Gastroenterol. 2007 Dec;42(12):1404-12. doi: 10.1080/00365520701514396.
Antiacid drugs, including omeprazole and ranitidine, were prescribed to Helicobacter pylori-infected subjects in combination with antibiotics during eradication treatment. Several reports suggest that these drugs have additional pharmacological properties, such as antineutrophil, antiapoptotic and antioxidant characteristics. The aim of this work was to study the effects of acid suppressive medication treatment in the H. pylori infection experimental model, focusing on possible additional pharmacological properties.
The ability of gastric acid suppression was assessed in pylorus-ligated animals. Gastric H. pylori colonization levels, myeloperoxidase (MPO) acitivity, macroscopic damage, Bax and Bcl-2 expression and DNA damage levels were assessed in C57BL/6-infected mice after treatment for one week with omeprazole (100 mg kg(-1)) or ranitidine (100 mg kg(-1)).
Omeprazole treatment increased bacteria colonization and MPO activity in mice stomachs. Both antiacid drugs efficiently improved macroscopic damage, although only omeprazole restored the expression of the antiapoptotic Bcl-2 protein in gastric mucosa of infected animals.
Some additional omeprazole-related properties, such as antineutrophil properties, were not observed in H. pylori-infected mice after one week of treatment, suggesting that this property is restricted to in vitro approaches. However, the antiapoptotic activity of omeprazole could be attributed to an ability to modify the protein expression of Bcl-2, decreased by H. pylori infection.
