Department of Gastroenterology and Metabolism, Graduate School of Medical Sciences, Nagoya City University, 1 Kawasumi, Mizuho, Nagoya, Aichi 467-8601, Japan.
J Clin Biochem Nutr. 2011 Mar;48(2):112-6. doi: 10.3164/jcbn.10-41. Epub 2011 Feb 26.
The pathophysiology of inflammatory bowel disease involves excessive immune effects of inflammatory cells against gut microbes. In genetically predisposed individuals, these effects are considered to contribute to the initiation and perpetuation of mucosal injury. Oxidative stress is a fundamental tissue-destructive mechanisms that can occur due to the reactive oxygen species and reactive nitrogen metabolites which are released in abundance from numerous inflammatory cells that have extravasated from lymphatics and blood vessels to the lamina propria. This extravasation is mediated by interactions between adhesion molecules including mucosal addressin cell adhesion molecule-1 and vascular cell adhesion molecule-1 on the surface of lymphocytes or neutrophils and their ligands on endothelial cells. Thus, reactive oxygen species and adhesion molecules play an important role in the development of inflammatory bowel disease. The present review focuses on the involvement of oxidative stress and adhesion molecules, in particular mucosal addressin cell adhesion molecule-1, in inflammatory bowel disease.
炎症性肠病的病理生理学涉及炎症细胞对肠道微生物的过度免疫反应。在遗传易感性个体中，这些效应被认为有助于粘膜损伤的启动和持续。氧化应激是一种基本的组织破坏机制，由于大量从淋巴和血管渗出到固有层的炎症细胞释放的活性氧和活性氮代谢物而发生。这种渗出是由粘附分子（包括淋巴细胞或中性粒细胞表面上的粘膜地址素细胞粘附分子-1 和血管细胞粘附分子-1 及其在内皮细胞上的配体）之间的相互作用介导的。因此，活性氧和粘附分子在炎症性肠病的发展中起重要作用。本综述重点介绍了氧化应激和粘附分子，特别是粘膜地址素细胞粘附分子-1，在炎症性肠病中的作用。
