| Theme |
Intestinal Mucosal Damage Induced by Drugs |
| Title |
Mechanisms of NSAID-induced Small Intestinal Mucosal Damage |
| Author |
Tomohisa Iwai |
Department of Gastroenterology, Kitasato University Graduate School of Medicine |
| Author |
Takafumi Ichikawa |
Department of Regulation Biochemistry of Kitasato University Graduate School of Medicine |
| Author |
Yukinobu Goso |
Department of Regulation Biochemistry of Kitasato University Graduate School of Medicine |
| Author |
Kazuhiko Ishihara |
Department of Regulation Biochemistry of Kitasato University Graduate School of Medicine |
| [ Summary ] |
Non-steroidal anti-inflammatory drugs (NSAIDs) induce small intestinal damage in experimental animals and humans. These effects of NSAIDs are considered to be mainly brought about by a deficiency of prostaglandins due to inhibition of cyclooxygenase. Furthermore, contractile activity, food in the intestines, neutrophil activation, nitric oxide overproduction, enterobacterial invasion, and mitochondrial dysfunction are postulated as the pathogenic elements of NSAID-induced small intestinal damage. The luminal surface of the gastrointestinal tract is covered by a viscoelastic mucous layer, which acts as a protective barrier against the intraluminal environment. NSAIDs cause quantitative and qualitative change in jejunal mucin, where most of the mucosal damage exists. In particular, sialomucin is considered to play an important role in regenerating the epithelium during the healing process. This article focuses on the role of mucins in intestinal damage and the pathogenesis of NSAID-induced small intestinal damage. |