Peptic ulcer is among the most serious gastrointestinal diseases in the world. Several orthodox drugs are employed for the treatment of the disease. Although these drugs are effective, they produce many adverse effects thus limiting their use. In recent years, there has been a growing interest in alternative therapies, especially those from plants due to their perceived relative lower side effects, ease of accessibility, and affordability. Plant medicines with ethnomedicinal use in peptic ulcer management need to be screened for their effectiveness and possible isolation of lead compounds. This requires use of appropriate animal models of various ulcers. The limited number of antiulcer models for drug development against gastric and duodenal ulcer studies has hindered the progress of targeted therapy in this field. It is, therefore, necessary to review the literature on experimental models used to screen agents with potential antigastroduodenal ulcer activity and explain their biochemical basis in order to facilitate their use in the development of new preventive and curative antiulcer drugs. Clinical trials can then be carried out on agents/drugs that show promise. In this paper, current in vivo animal models of ulcers and the pathophysiological mechanisms underlying their induction, their limitations, as well as the challenges associated with their use have been discussed. 1. Introduction Peptic ulcer diseases comprise heterogeneous disorders, which manifest as a break in the lining of the gastrointestinal mucosa bathed by acid and pepsin. It is the most predominant of the gastrointestinal diseases [1, 2] with a worldwide prevalence of about 40% in the developed countries and 80% in the developing countries. It is generally recognized that peptic ulcer is caused by a lack of equilibrium between the gastric aggressive factors and the mucosal defensive factors [3]. Based on site of attack, peptic ulcer may be classified as oesophageal, duodenal, or gastric. The etiology of gastroduodenal ulcers is influenced by various aggressive and defensive factors such as acid-pepsin secretion, parietal cell, mucosal barrier, mucus secretion, blood flow, cellular regeneration and endogenous protective agents (prostaglandins and epidermal growth factors) [4]. According to Peckenpaugh and Poleman [5], some other factors, such as bad dietary habits, excessive intake of nonsteroidal anti-inflammatory agents, stress, hereditary predisposition and Helicobacter pylori infection, which is reported to account for more than 70% of cases, are responsible for the development of
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