Liu Yanping, Li Tianming, Niu Changping, Yuan Zhengwei, Sun Siyu, Liu Dongyan
Department of Gastroenterology and Medical Research Center, Liaoning Key Laboratory of Research and Application of Animal Models for Environmental and Metabolic Diseases, ShengJing Hospital of China Medical University, SanHao Street No. 36, HePing District, Shenyang, 110000, Liaoning, China.
Department of Pathology, Cancer Hospital of China Medical University, Cancer Hospital of Dalian University of Technology, Liaoning Cancer Hospital & Institute, No. 44 Xiaoheyan Road, Dadong District, Shenyang, 110042, Liaoning, People's Republic of China.
Mol Med. 2025 Jan 3;31(1):1. doi: 10.1186/s10020-024-00993-7.
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.
由于高氧诱导的肠道损伤机制可能导致新生儿并发症，对该机制缺乏了解已引起了相当大的关注。本研究旨在探讨高氧诱导的肠道组织氧化损伤与铁死亡之间的关系，并研究高氧通过铁死亡调节炎症的机制。该研究系统地评估了高氧在体外和体内对肠道上皮细胞氧化应激、线粒体损伤、铁死亡和炎症的影响。结果表明，铁死亡参与了高氧引起的肠道氧化损伤，并受Nrf2调控。此外，高氧诱导的氧化损伤通过上调COX-2/PGE2/EP2信号通路，通过铁死亡调节炎症。这些发现对未来临床预防和治疗高氧治疗引起的新生儿器官损伤的方法具有重要意义。
