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Burns Trauma, 2022, 10, tkac008 doi.org/10.1093/burnst/tkac008 Research ArticleResearch ArticleThe Notch pathway attenuates burn-induced acute lung injury in rats by repressing reactive oxygen speciesWeixia Cai , Kuo Shen , Peng Ji , Yanhui Jia , Shichao Han, Wanfu Zhang, Xiaolong Hu, Xuekang Yang, Juntao Han and Dahai HuDepartment of Burns and Cutaneous Surgery, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, ChinaCorrespondence.Tetrabutylammonium Purity & Documentation Dahai Hu, Email: hudahaidoc@163; Juntao Han, E-mail: hanjt@fmmu.PMID:23659187 edu.cn; Xuekang Yang, E-mail: yangxuekangburns@163These authors contributed equally to this work as co-first authors.Received 23 September 2021; Revised two February 2022; Editorial choice 8 FebruaryAbstractBackground: Acute lung injury (ALI) is a prevalent complication following severe burns. The underlying mechanisms of ALI are incompletely understood; therefore, accessible treatment options are not adequate to repair the lung tissue soon after ALI. Methods: To investigate the partnership between the Notch pathway and burn-induced lung injury, we established a rat burn injury model by scalding and verified lung injury by means of lung injury evaluations, like hematoxylin and eosin (H E) staining, lung injury scoring, bronchoalveolar lavage fluid and wet/dry ratio analyses, myeloperoxidase immunohistochemical staining and reactive oxygen species (ROS) accumulation analysis. To explore regardless of whether burn injury impacts Notch1 expression, we detected the expression of Notch1 and Hes1 after burn injury. Then, we extracted pulmonary microvascular endothelial cells (PMVECs) and conducted Notch pathway inhibition and activation experiments, via a -secretase inhibitor (GSI) and OP9-DLL1 coculture, respectively, to confirm the regulatory impact on the Notch pathway on ROS accumulation and apoptosis in burnserum-stimulated PMVECs. To investigate the regulatory impact from the Notch pathway on ROS accumulation, we detected the expression of oxidative-stress-related molecules for example superoxide dismutase, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) two, NOX4 and cleaved caspase-3. NOX4-specific little interfering RNA (siRNA) and the inhibitor GKT137831 were utilized to verify the regulatory effect from the Notch pathway on ROS by means of NOX4. Results: We effectively established a burn model and revealed that lung injury, excessive ROS accumulation and an inflamm.
