Effect of Ranitidine on Taurocholate-, Ethanol-, and Indomethacin-Induced Damage to Gastric Epithelial Cells in vitro

Abstract

We evaluated whether ranitidine protects gastric epithelial cells against damage induced by sodium taurocholate, ethanol or indomethacin, under conditions independent of its acid inhibitory effect as well as of systemic factors. We also studied the role of prostaglandins and sulfhydryls in any such protection. Ranitidine significantly reduced the amount of damage induced by taurocholate, but did not afford protection against ethanol- and indo-methacin-induced damage. Incubation with ranitidine did not increase PGE₂ production by cultured cells nor did it affect the cellular content of sulfhydryls. The protective effect of ranitidine against taurocholate was not prevented by indomethacin or by the sulfhydryl blocker, N-ethylmaleimide. In conclusion, this in vitro study confirms that H₂ blockers such as ranitidine have a limited cytoprotective ability independent of acid secretion, which is not as extensive as agents such as prostaglandins and sulfhydryls. This may be because prostaglandins and sulfhydryls play no role in the protective effect of ranitidine.

Antioxidant effect of dry olive (Olea europaea L.) leaf extract on ethanol-induced gastric lesions in rats

“…The mechanism of action of ranitidine is well known. Furthermore, an in vitro study confirmed that H 2 blockers such as ranitidine have limited cytoprotective ability independent of acid secretion [42]. Figure 3 shows MDA concentration in normal gastric mucosa and in gastric mucosa of non-pretreated rats and rats pretreated with OLE and ranitidine.…”