| Summary: | Peptic ulcer disease, usually seen in the stomach and proximal duodenum, is a disease that can be seen in individuals of different age groups due to a wide variety of infectious and non-infectious causes. The understanding of the etiopathogenesis of peptic ulcer disease is an important factor in the prevention, treatment and management of this disease. Although there are several factors known to cause gastric ulcers, the mechanism of mucosal injury in the stomach related to gastric ulcers has not been fully clarified. Attempts to protect against a variety of environmental factors of gastric mucosa through prostaglandins play an active role in the protection of gastric ulcer. Numerous investigations have been conducted on gastric injury studies using necrotizing agents, nonsteroidal anti-inflammatory drugs and cold restriction stress models for the protective effect of some prostaglandins in the stomach. This allows removal of the gastric mucosa prostaglandin E2 in the development and progression of peptic ulcers has been shown to be a significant etiological factor. In the light of all this information, the goal of this review is discussing the etiopathogenesis of peptic ulcers and prostaglandin relationship as a whole, and thus to provide the researchers with a thorough knowledge of future studies. In conclusion, it can be said that prostaglandins are directly or indirectly related to some ulcerogenic and protective factors, especially stress, hormonal response, gastric acid, and mucus, and they also play important roles in the etiopathogenesis of peptic ulcer disease.
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