Abstract

Ulcer is the most common undesirable result of using non-steroid anti-inflammatory drugs such as indomethacin. In the present study, osajin was experimentally used on indomethacin-induced gastric ulcer in rats. Osajin was purified from Maclura pomifera (Raf.) C. K. Schneid fruits by using the chromatographic methods. Thirty six rats were divided into six groups as follows: healthy (control), IND (indomethacin), RAN (ranitidine, 25 mg/kg), OSJ 100 (osajin, 100 mg/kg), OSJ 200 (200 mg/kg) and OSJ 400 (osajin, 400 mg/kg). Following a 24-h fasting, IND was administered to the treatment groups at a dose of 25 mg/kg. RAN and OSJ were given orally to rats following 5 min of IND administration. Then, gastric tissues were taken 6 h after the IND administration. Determination of the ulcer area, pathological evidence, and biochemical indices such as lipid peroxidation, superoxide dismutase, glutathione, and catalase were performed. IND generated diffuse ulcer areas, severe hyperaemia, oedema, necrotic epithelium, and mononuclear cell infiltration in the mucosa, and significantly increased lipid peroxidation while also decreasing the glutathione concentration, superoxide dismutase and catalase activities of the tissue. OSJ and RAN showed significant amelioration on ulcer area and biochemical indices. Therefore, OSJ may be potentially therapeutic for gastric ulcers.

Highlights

  • Ulcer is a limited or widespread mucosal necrotic wound that can bleed and involve all the tissue layers as a consequence of damage to the protective structure of the gastrointestinal (GI) tracts of mammals (Laine 2016)

  • OSJ and RAN administrations markedly decreased the ulcer areas compared to the IND group (P < 0.05)

  • Necrotic epithelial cells reached up to lamina muscularis, mild mononuclear cell infiltration and hyperaemia in vessels were observed in the IND group (Plate VII, Fig. 4b)

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Summary

Introduction

Ulcer is a limited or widespread mucosal necrotic wound that can bleed and involve all the tissue layers as a consequence of damage to the protective structure of the gastrointestinal (GI) tracts of mammals (Laine 2016). Non-steroidal anti-inflammatory drugs (NSAIDs) have been reported to be the most important cause of GI ulcers after H. pylori (Bayir et al 2006). It has been reported that the ROS generate oxidized products via attacking the phospholipids of the cell membrane. They increase the tissue damage by causing deterioration in the structure of enzymes, proteins, and receptors (Slater et al 1987). OSJ has previously been reported to have some properties such as inhibition of COX-2 expression in skin cell (Kim et al 2017) and DNA protectivity (Diopan et al 2008), its effect on the GI system has not been investigated. Schneid fruits on the indomethacin-induced gastric damage in rats were investigated by performing macroscopic, histopathologic and biochemical examinations

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