Nuclear factor erythroid 2-related factor 2 potentiates the generation of inflammatory cytokines by intestinal epithelial cells during hyperoxia by inducing the expression of interleukin 17D

Liu, Xuying; Li, Tianming; Liu, Yanping; Sun, Siyu; Liu, Dongyan

doi:10.1016/j.tox.2021.152820

Cited by 7 publications

(2 citation statements)

References 36 publications

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“…Liu et al found that Nrf2 and IL-17D expression increased significantly under hyperoxia conditions. Furthermore, the expression of IL-17D was further increased after Nrf2 was activated with tert-butylhydroquinone (TBHQ) [ 34 ]. This suggests that during hyperoxia, intestinal epithelial cells and immune cells respond to the damage caused by hyperoxia by promoting the inflammatory response through IL-17D (shown in Figure 1 ).…”

Section: Immune Barriermentioning

confidence: 99%

Mechanism of Neonatal Intestinal Injury Induced by Hyperoxia Therapy

Liu

2022

Journal of Immunology Research

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High concentration oxygen is widely used in the treatment of neonates, which has a significant effect on improving blood oxygen concentration in neonates with respiratory distress. The adverse effects of hyperoxia therapy on the lung, retina, and neurodevelopment of newborns have been extensively studied, but less attention has been paid to intestinal damage caused by hyperoxia therapy. In this review, we focus on the physical, immune, and microorganism barriers of the intestinal tract and discuss neonatal intestinal tract damage caused by hyperoxia therapy and analyze the molecular mechanism of intestinal damage caused by hyperoxia in combination with necrotizing enterocolitis.

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Section: Immune Barriermentioning

confidence: 99%

Mechanism of Neonatal Intestinal Injury Induced by Hyperoxia Therapy

Liu

2022

Journal of Immunology Research

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“…Additionally, Nrf2 can eliminate ROS through glutathione (GSH) metabolism and regulate the ROS level by controlling the steady ow of free ferrous ions [19]. Our previous research showed that in hyperoxia Nrf2 increased to neutralize much ROS in intestinal epithelial cells [20]. So Nrf2 might inhibite ferroptosis to protect intestinal epithelial cells in hyperoxia.…”

Section: Introductionmentioning

confidence: 99%

Hyperoxia-activated Nrf2 regulates ferroptosis in intestinal epithelial cells and intervenes in inflammatory reaction through COX-2/PGE2/EP2 pathway

Liu,

Li,

Niu

et al. 2024

Preprint

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The lack of knowledge about the mechanism of hyperoxia-induced intestinal injury has attracted considerable attention, due to the potential for this condition to cause neonatal complications. This study aimed to explore the relationship between hyperoxia-induced oxidative damage and ferroptosis in intestinal tissue and investigate the mechanism by which hyperoxia regulates inflammation through ferroptosis. The study systematically evaluated the effects of hyperoxia on oxidative stress, mitochondrial damage, ferroptosis, and inflammation of intestinal epithelial cells both in vitro and in vivo. The results showed that ferroptosis was involved in intestinal oxidative damage caused by hyperoxia and was regulated by Nrf2. Moreover, hyperoxia-induced oxidative damage regulated inflammation through ferroptosis by upregulating the COX-2/PGE2/EP2 signaling pathway. These findings have important implications for future clinical prevention and therapeutic approaches to neonatal organ injury caused by hyperoxia treatment.

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IL-17D affects the chemokines and chemokine receptors of intestinal epithelial cells under hyperoxia

Liu

et al. 2022

International Immunopharmacology

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Nuclear factor erythroid 2-related factor 2 potentiates the generation of inflammatory cytokines by intestinal epithelial cells during hyperoxia by inducing the expression of interleukin 17D

Cited by 7 publications

References 36 publications

Mechanism of Neonatal Intestinal Injury Induced by Hyperoxia Therapy

Mechanism of Neonatal Intestinal Injury Induced by Hyperoxia Therapy

Hyperoxia-activated Nrf2 regulates ferroptosis in intestinal epithelial cells and intervenes in inflammatory reaction through COX-2/PGE2/EP2 pathway

IL-17D affects the chemokines and chemokine receptors of intestinal epithelial cells under hyperoxia

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