Gastro-protective and anti-acidic effects of Corchorus trilocularis Linn against diclofenac- induced gastric ulcers.

Abstract

Ethnopharmacological Relevance:Corchorus trilocularis Linn leaves are consumed as green leafy vegetables that are boiled and used as relish, or potherb by some rural communities in Eastern Africa for the treatment of stomach ulcers. Aim:This study investigated the gastro-protective effects of Corchorus trilocularis Linn (local name ‘mrenda’), a popularly consumed vegetable in Kenya, on diclofenac-induced gastric ulcers and established its possible mechanisms of action. Methods: In the in-vivo study, thirty six Sprague dawley rats of either sex weighing 150-200 grams were randomly assigned into a normal control (distilled water), negative control (distilled water plus diclofenac sodium), treatment (200 and 400 mg/kg Corchorus trilocularis Linn plus diclofenac sodium), positive control group (omeprazole plus diclofenac sodium), or comparison group (400 mg/kg aqueous leaf extract of spinach). The ulcer index, total acidity, volume, pH of gastric secretions, and gastric morphology were assessed. In the in-vitro anti-acidity study, a rat stomach was perfused with Kreb’s solution and the pH of the mucosal perfusate measured using a digital pH meter for 1 hour after exposure to histamine, acetylcholine, or pre-treatment with 400 mg/kg of theextract prior to addition the acid secretagogues. Results: The extract, significantly reduced the ulcer index and total acidity in comparison to the diclofenac group. The high dose extract also increased the gastric pH and had cytoprotective effects. However, it did not significantly affect the volume of gastric secretions. In the in-vitro study, the extract significantly inhibited histamine and acetylcholine stimulated gastric acid secretions as analyzed by the areas under curve for pH against time. Conclusions: The gastro-protective effects of Corchorus trilocularis Linn against diclofenac induced gastric ulcers are; therefore, mediated through preservation of the gastric mucosal barrier, increase in gastric pH, and inhibition of gastric acid secretion through the histamine H2 and acetylcholine M3 extracellular pathways on the parietal cell.