不同氧浓度下氧化应激在未成熟肠道中的作用机制

The mechanism of oxidative stress in the immature gut under different oxygen concentrations

不同氧浓度条件下所致的氧化应激会对新生儿及早产儿的未成熟肠道造成损伤。新生儿尤其是早产儿肠道发育不全,免疫功能不成熟,对氧化应激的易感性增加,易发生肠道炎性疾病。缺氧或高氧均可能引发氧化应激,导致肠道损伤。组织学变化包括肠道屏障损伤、肠上皮细胞水样变性以及杯状细胞和绒毛减少,还会引起肠道菌群失调。缺氧诱导的肠道损伤受多种信号通路的影响,包括CRF-TLR4、Grx1-HIF-VEGF、NLRP3-Caspase-1信号通路、miRNA-SIRT轴。高氧引发的肠道损伤则与TLR4/NF-κB信号通路、Nrf2/IL-17D轴、ASK1-MAPK级联有很大关系。该文综述缺氧或高氧诱导肠道损伤的组织学变化和分子途径,以建立潜在干预的框架。

Oxidative stress by different oxygen concentrations can cause damage to the immature intestinal tract of newborns and preterm infants.Newborns,especially premature infants,have underdeveloped intestinal tracts,immature immune function,increased susceptibility to oxidative stress,and are prone to intestinal inflammatory diseases.Both hypoxia and hyperoxia can trigger oxidative stress,leading to intestinal damage.Histological changes include damage to the intestinal barrier,watery degeneration of the intestinal epithelium,and reduced goblet cells and villi.Hypoxia-induced intestinal injury is affected by a variety of signaling pathways including CRF-TLR4,Grx1-HIF-VEGF,NLRP3-Caspase-1,and miRNA-SIRT axis.The intestinal injury induced by hyperoxia is closely related to TLR4/NF-κB signaling pathway,Nrf2/IL-17D axis,and ASK1-MAPK cascade.This review focuses on the histological changes and molecular pathways of hypoxic or hyperoxic-induced intestinal injury to establish a framework for potential interventions.