Abstract

The present study was designed to investigate the effect of Mimusops elengi (Sapotaceae) against experimental gastric ulcers. The 50% alcoholic extract of Mimusops elengi (Ext E) and its different fractions namely ethyl acetate (Ext E 1), n-butanol (Ext E 2), methanol (Ext E 3) and aqueous (Ext E 4) were studied (p.o.) against ethanol-induced gastric damage. Ext E 1 was also studied in ethanol-induced, pylorus-ligated and water-immersion plus stress-induced gastric ulcer models. Ranitidine HCl (80 mg kg −1) was used as a reference standard. In ethanol-induced gastric ulcer model, pantoprazole (20 mg kg −1) was also used as a reference standard. Ext E 1 tested in mice up to the dose of 5000 mg kg −1 (p.o.) did not produce any sign of toxicity. Ext E at the doses of 50, 100, 300 and 500 mg kg −1 and its different fractions (100 mg kg −1) showed reduction in gastric ulceration ( P<0.05). Ext E 1 at the doses of 10, 50 and 100 mg kg −1 showed dose-dependent inhibition of gastric lesions against ethanol-induced gastric damage. In 19 h pylorus-ligated animals, Ext E 1 at 50 and 100 mg kg −1 doses showed significant reduction in ulcer index ( P<0.05). Significant reduction was also observed in total acidity, volume of gastric acid secretion, total acid output and pepsin activity ( P<0.05) when compared with the control group. Besides, Ext E 1 showed increase in the mucosal glycoproteins that was evident from significant rise in total carbohydrates to protein ratio (TC:PR ratio) ( P<0.05), which is an indication of mucin activity. Ext E 1 also showed protection against water-immersion plus stress-induced gastric lesions that was evident from dose-dependent decrease in ulcer index ( P<0.05), score for intensity ( P<0.05) and total lesion area ( P<0.05) when compared with the control group. It can be concluded from our study that Ext E 1 possesses anti-ulcer activity against experimental gastric ulcers. The mechanism of anti-ulcer activity can be attributed to decrease in gastric acid secretory activity along with strengthening of mucosal defensive mechanisms.

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