Abstract
Purpose: Honey is widely used all over the world in complementary and alternative medicine in various disorders, including gastrointestinal lesions. Unfortunately, the therapeutic potential of honey has so far been neglected in modern medicine owing to a lack of systematic scientific studies. Recent studies using different models of experimentally induced acute and chronic gastric lesions in rats have demonstrated the gastric protection effects and molecular mechanisms of honey. As ammonia is highly cytotoxic, its production by urease of Helicobacter pylori makes it an important aggressive factor in mucosal injury. The present work was undertaken to evaluate potential gastric protection by honey and its possible mechanism(s) against ammonia‐induced gastric lesions in rats.
Materials and Methods: Twenty‐four hour fasted rats were given 1 ml of ammonium hydroxide 1% intragastrically and were killed 1 hour later under deep ether anaesthesia. The gastric lesion index was calculated according to the method of Takaishi et al. Non‐protein sulphydryl levels were measured spectrophotometrically.
Results: In control animals, the administration of ammonium hydroxide produced red and black linear lesions along the folds in the greater curvature and to the antrum. There was also significant depletion of glandular non‐protein sulphydryl levels. On the other hand, oral administration of honey or sucralfate 30 min before ammonium hydroxide dose‐dependently reduced the severity of gastric mucosal lesions and reversed the changes in glandular non‐protein sulphydryl levels induced by ammonium hydroxide. Carbohydrate components seem to have no role in the protective mechanism.
Conclusion: The results indicate a modulator role of endogenous non‐protein sulphydryls in the protective mechanisms of both honey and sucralfate. This unique property of honey may be important in the management of Helicobacter pylori‐associated mucosal lesions.