The role of ROS-pyroptosis in PM 2.5 induced air-blood barrier destruction.

Autor: Wei M; College of Medical Laboratory, Dalian Medical University, Dalian, Liaoning Province, 116044, PR China; Linfen Meternity & Child Healthcare Hospital, Linfen, Shanxi Province, 041000, PR China., Cong Y; College of Medical Laboratory, Dalian Medical University, Dalian, Liaoning Province, 116044, PR China., Lei J; College of Medical Laboratory, Dalian Medical University, Dalian, Liaoning Province, 116044, PR China., Du R; College of Medical Laboratory, Dalian Medical University, Dalian, Liaoning Province, 116044, PR China., Yang M; Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, 116023, PR China., Lu X; First Affiliated Hospital, Dalian Medical University, Dalian, Liaoning Province, 116000, PR China., Jiang Y; Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, 116023, PR China., Cao R; Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, 116023, PR China., Meng X; Department of Cognitive Neuroscience, Centre for Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, the Netherlands., Jiang Z; Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, 116023, PR China., Song L; College of Medical Laboratory, Dalian Medical University, Dalian, Liaoning Province, 116044, PR China. Electronic address: evasong@dmu.edu.cn.
Jazyk: angličtina
Zdroj: Chemico-biological interactions [Chem Biol Interact] 2023 Dec 01; Vol. 386, pp. 110782. Date of Electronic Publication: 2023 Oct 24.
DOI: 10.1016/j.cbi.2023.110782
Abstrakt: Fine particulate matter (PM 2.5 ) has attracted increasing attention due to its health-threatening effects. Although numerous studies have investigated the impact of PM 2.5 on lung injuries, the specific mechanisms underlying the damage to the air-blood barrier after exposure to PM 2.5 remain unclear. In this study, we established an in vitro co-culture system using lung epithelial cells and capillary endothelial cells. Our findings indicated that the tight junction (TJ) proteins were up-regulated in the co-cultured system compared to the monolayer-cultured cells, suggesting the establishment of a more closely connected in vitro system. Following exposure to PM 2.5 , we observed damage to the air-blood barrier in vitro. Concurrently, PM 2.5 exposure induced significant oxidative stress and activated the NLRP3 inflammasome-mediated pyroptosis pathway. When oxidative stress was inhibited, we observed a decrease in pyroptosis and an increase in TJ protein levels. Additionally, disulfiram reversed the adverse effects of PM 2.5 , effectively suppressing pyroptosis and ameliorating air-blood barrier dysfunction. Our results indicate that the oxidative stress-pyroptosis pathway plays a critical role in the disruption of the air-blood barrier induced by PM 2.5 exposure. Disulfiram may represent a promising therapeutic option for mitigating PM 2.5 -related lung damage.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2023 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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