缺氧在肠黏膜炎症损伤过程中的病理生理机制

Role of hypoxic injury in pathophysiology of intestinal mucosal inflammation

细胞缺氧影响细胞的正常代谢,影响组织器官正常功能,导致疾病发生.在实验小鼠模型和人类炎症性肠病(inflammatory bowel disease,IBD)患者的肠黏膜上均可见不同程度的缺氧,氧供给和氧消耗之间的平衡受到破坏.机体缺氧时,一些低氧诱导因子,如低氧诱导因子(hypoxia-inducible factor,HIF)-1、HIF-2和HIF-3,能够通过不同的调节机制调控不同的生理反应.脯氨酰羟化酶(proline hydroxylasedomain,PHD)是一种双加氧酶的氧感受器,通过催化HIF脯氨酸残基发生羟化反应介导其降解.IBD与缺氧有着密切的联系,在IBD中如何提高机体对缺氧的反应逐渐被研究人员重视,并被看做为一种新颖的治疗理念,本文就缺氧在IBD肠道黏膜炎症损伤过程中的病理生理变化进行综述分析.

Hypoxia influences the normal metabolism of cells and normal functions of organs, eventually causing diseases. Various degrees of hypoxia can be seen in the intestinal mucosa of both ex- perimental mouse models and patients with in- flammatory bowel disease （IBD）, whose oxygen supply and oxygen consumption are damaged. A number of hypoxia inducible factors, such as HIF-1, HIF-2 and HIF-3, can regulate different physiological responses via different mechanisms. Proline hydroxylasedomain （PHD） is a two-diox- ygenase oxygen sensor that can mediate degra- dation of proline residues of HIFs. IBD is closely related to hypoxia. In recent years, researchers have paid more attention to improving the body＇s reaction to hypoxia in IBD, which is considered a novel treatment concept. This review will analyze the role of hypoxic injury in the pathophysiology of intestinal mucosal inflammation in IBD.