INVESTIGATING THE GASTROPROTECTIVE EFFECT OF MORINA LONGIFOLIA AGAINST INDOMETHACIN-INDUCED GASTRIC ULCER

Peptic ulcer disease (PUD) can be defined as the presence of a deep destruction of the stomach lining or mucosa or duodenum, reaching beyond the muscularis mucosa, specifically to the muscle layer owing to the environmental gastric acid synthesis.[1] The primary cause of peptic ulcer is infection with Helicobacter pylori (H. pylori), a bacterium that weakens the protective mucosal lining of the stomach, making it susceptible to damage by stomach acid.[2] Another major cause is the prolonged use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen, which interfere with the production of prostaglandins, compounds that help maintain the protective mucus barrier.[3,4] Peptic ulcer symptoms can range from mild to severe, but they usually include nausea, bloating, heartburn, searing sensation in the stomach (which is worst when the stomach is empty or at night), vomiting, and lack of appetite. Some of the complications that can develop in more severe cases include bleeding ulcers, which can cause blood in the stool and vomiting, perforation, which is characterized by severe abdominal pain caused by the ulcer creating a hole in the intestines or stomach, and gastric outlet obstruction, which is characterized by food blockage and persistent vomiting.[5] Study data suggest the prevalence rate of this disease covers four million people worldwide annually and has an estimated lifetime prevalence of 5−10% in the general population. While the overall occurrence of PUD has declined significantly over the last several decades, but the occurrence of its consequences has stayed the.[6] In 2019, the global prevalence of PUD was approximately 8.09 million, representing a 25.82% increase from 1990.[7] NSAIDs are well documented as producing upper gastrointestinal (GI) problems, ranging from dyspeptic symptoms in up to 40% to life-threatening complex ulcers (haemorrhage, perforation, or pyloric blockage). Gastroduodenal (GD) damage associated to NSAID usage is regarded to be the most prevalent and, in aggregate, the most devastating consequence of any pharmacological treatment. The incidence of peptic ulceration in chronic NSAID users is 20–30%, with gastric ulcers roughly six times more prevalent than duodenal ulcers. The risk of hospitalization for major upper GI problems (bleeding or perforation) with NSAID usage is 1–2% per year.[8]