GASTRIC ANTIULCER AND ULCER HEALING EFFECTS OF PUNICA GRANATUM L. PEEL EXTRACT IN RATS: ROLE OF OFFENSIVE AND DEFENSIVE MUCOSAL FACTORS AND OXIDATIVE STRESS

Indal Chauhan,Mayank Gangwar,Ankita Sharma,Raj Kumar Goel,Amit Singh,Manish Kumar Gautam

doi:10.22159/ijpps.2017v9i5.9851

Abstract

Objective: The present work incorporates the study of gastric antiulcer and ulcer healing effects of dried Punica granatum (PG) peel 50% ethanol extract (PGE) in rats.Methods: PGE (100 mg/kg) was administered orally once daily to rats either before or after induction of gastric ulcers (GU) for 7 d. Antiulcer effects of PGE were seen against acute GU, induced by pylorus ligation (PL), cold restraint stress (CRS), aspirin and ethanol while, ulcer healing in acetic acid (AA)-induced chronic GU in rats. Ulcer index (UI), gastric juice volume, acid-pepsin and mucin secretions and gastric mucosal glycoproteins, free radicals (LPO and NO) and antioxidants (SOD and GSH) were estimated.Results: PGE showed a decrease in UI in all GU models (45.6 to 79.7%, P<0.05 to P<0.001) indicating both protective and healing effects. PGE showed little or no effects on volume, acid-pepsin concentration and output but increased mucin secretion (55.1%, P<0.05) and mucosal glycoproteins (35.7%, P<0.05) in PL rats. CRS rats showed an increase in LPO and NO (48.4 to 58.3%, P<0.01) and SOD (21.8%, P<0.01) but decrease in GSH and CAT (33.1 to 44.8%, P<0.01 to P<0.001) compared with unstressed rats. PGE-treated CRS rats showed a decrease in LPO and NO (44.1 to 61.2, P<0.01 to P<0.001) and SOD (13.2%, P<0.01) and increase in GSH and CAT (43.8 to 48.7%, P<0.01 to P<0.001) compared with CRS rats.Conclusion: PGE seemed to have ulcer cytoprotective effects due to enhanced mucosal resistance and reduction in oxidative mucosal damage possibly via high antioxidant activity.

Highlights

Gastroduodenal ulceration is defects in the gastrointestinal mucosa that may extend through the muscularis mucosa
The acid peptic injury is necessary for ulcers to form, acid secretion is normal in almost all the patients with gastric ulcers and increased in only one-third of patients with duodenal ulcers indicating the role played by defence mechanisms in preventing ulceration
PGE showed a dose-dependent decrease in ulcer index against cold restraint stress (CRS)-induced gastric ulcers (GU) (Control CMC Ulcer index (UI)-27.4±3.09; PGE-20.8 to 57.3% decrease, P

Summary

Introduction

Gastroduodenal ulceration is defects in the gastrointestinal mucosa that may extend through the muscularis mucosa. Peptic ulcer disease occurs as a result of an imbalance between offensive (acid, pepsin, bile, oxidative stress, etc.) and defensive (mucus and bicarbonate secretion, prostaglandins, blood flow, antioxidant status and the processes of restitution and regeneration after cellular injury) factors in the gastroduodenal mucosa [1]. H. pylori infection, NSAIDs, and acid secretory abnormalities are the major factors that disrupt this equilibrium. A defect in bicarbonate production and in turn, acid neutralization in the duodenal bulb, is seen in patients with duodenal ulcer disease. A small percentage of ulcers are related to H. pylori infection or NSAID use

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