Research Article Pathophysiological Mechanisms and Preclinical Models of Peptic Ulcer

A Peptic ulcer is a mucosal lesion of the stomach or duodenum in which the acid and pepsin play major pathogenic roles. The major forms of peptic ulcer are gastric ulcer and duodenal ulcer, both of which are chronic diseases often caused by Helicobacter pylori. The term peptic ulcer also encompasses gastric ulcers and duodenal ulcers associated with stress or the ingestion of drugs, most commonly aspirin and non-steroidal anti-inflammatory drugs (NSAIDs). Ulcer associated with Zollinger-Ellison Syndrome (ZES), caused by gastrin secreting is also considered a form of peptic ulcer. Whether an ulcer develops, depends on the balance between aggressive factors ( mainly gastric acid and pepsin) and factor that participate in mucosal defense or resistance to ulceration. Peptic ulcer develops when gastro duodenal mucosal defenses are unable to protect the epithelium from the corrosive effects of acid and pepsin. Gastric acid catalyses the cleavage of inactive pepsinogen molecules to proteolytically active pepsins and also provides the low pH for pepsin activity. Peptic ulcer effect of plant drugs and herbal formulations are studied against chemicals ( ethanol, acetic acid, histamine), drugs (dimaprit, indomethacin, aspirin, reserpine) and stress induced ulcer in rats as they virtually mimic any form of occurring gastric ulcer in stomach. The level of pH, total acidity, ulcer index reflects damage to stomach mucus as well as protective effect of plant drugs.