Tian Tian, Wang Ziling, Zhang Jinhua
College of Life Science and Bioengineering, Beijing Jiaotong University, Beijing 100044, China.
Oxid Med Cell Longev. 2017;2017:4535194. doi: 10.1155/2017/4535194. Epub 2017 Jun 28.
Inflammatory bowel disease (IBD) is a chronic gastrointestinal disease whose incidence has risen worldwide in recent years. Accumulating evidence shows that oxidative stress plays an essential role in the pathogenesis and progression of IBD. This review highlights the generation of reactive oxygen species (ROS) and antioxidant defense mechanisms in the gastrointestinal (GI) tract, the involvement of oxidative stress signaling in the initiation and progression of IBD and its relationships with genetic susceptibility and the mucosal immune response. In addition, potential therapeutic strategies for IBD that target oxidative stress signaling are reviewed and discussed. Though substantial progress has been made in understanding the role of oxidative stress in IBD in humans and experimental animals, the underlying mechanisms are still not well defined. Thus, further studies are needed to validate how oxidative stress signaling is involved in and contributes to the development of IBD.
炎症性肠病(IBD)是一种慢性胃肠道疾病,近年来其发病率在全球范围内呈上升趋势。越来越多的证据表明,氧化应激在IBD的发病机制和进展中起着至关重要的作用。本综述重点介绍了胃肠道中活性氧(ROS)的产生和抗氧化防御机制、氧化应激信号在IBD发生和进展中的作用及其与遗传易感性和黏膜免疫反应的关系。此外,还对针对氧化应激信号的IBD潜在治疗策略进行了综述和讨论。尽管在理解氧化应激在人类和实验动物IBD中的作用方面已经取得了重大进展,但其潜在机制仍未完全明确。因此,需要进一步研究来验证氧化应激信号是如何参与并促进IBD发展的。