Anti-ulcerogenic effect of osajin on indomethacin-induced gastric damage in rats

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. Ranitidine, gastric ulcer, Maclura pomifera 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). The most common causes of a GI ulcer in mammals are Helicobacter pylori, drugs, alcohol, and stress conditions such as cold or hot temperatures. 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). Across the world, NSAIDs such as aspirin, ibuprofen, and indomethacin are frequently used as medication for inflammation, pain and rheumatoid arthritis both in human and animal patients. The NSAIDs produce their curative effects via the inhibition on COX (cyclooxygenase) enzyme activity in cells. However, the inhibition of the COX system, which is related to arachidonic acid, causes reduced prostaglandin E2 (PGE2) synthesis that is part of the GI protective system (Rainsford 1988). In recent studies, reactive oxygen species (ROS) have been shown to be an important factor in the pathophysiology of GI ulcers (Atalay et al. 2015; Bozkurt et al. 2017), inducing oxidative stress in cells (Pandır et al. 2019). It has been reported that the ROS generate oxidized products via attacking the phospholipids of the cell membrane. They also increase the tissue damage by causing deterioration in the structure of enzymes, proteins, and receptors (Slater et al. 1987). ACTA VET. BRNO 2020, 89: 391–400; https://doi.org/10.2754/avb202089040391 Address for correspondence: Huseyin Serkan Erol Department of Biochemistry Faculty of Veterinary Medicine, Kastamonu University Kastamonu, 37200, TURKEY Phone: +90 366 280 5116 E-mail: hserol@kastamonu.edu. tr http://actavet.vfu. cz/