Literature DB >> 27560977

Argon Preconditioning Protects Airway Epithelial Cells against Hydrogen Peroxide-Induced Oxidative Stress.

Christina Hafner1, Hong Qi, Lourdes Soto-Gonzalez, Katharina Doerr, Roman Ullrich, Eva Verena Tretter, Klaus Markstaller, Klaus Ulrich Klein.   

Abstract

BACKGROUND: Oxidative stress is the predominant pathogenic mechanism of ischaemia-reperfusion (IR) injury. The noble gas argon has been shown to alleviate oxidative stress-related myocardial and cerebral injury. The risk of lung IR injury is increased in some major surgeries, reducing clinical outcome. However, no study has examined the lung-protective efficacy of argon preconditioning. The present study investigated the protective effects of argon preconditioning on airway epithelial cells exposed to hydrogen peroxide (H2O2) to induce oxidative stress.
METHODS: A549 airway epithelial cells were treated with a cytotoxic concentration of H2O2 after exposure to standard air or 30 or 50% argon/21% oxygen/5% carbon dioxide/rest nitrogen for 30, 45 or 180 min. Cells were stained with annexin V/propidium iodide, and apoptosis was evaluated by fluorescence-activated cell sorting. Protective signalling pathways activated by argon exposure were identified by Western blot analysis for phosphorylated candidate molecules of the mitogen-activated protein kinase and protein kinase B (Akt) pathways.
RESULTS: Preconditioning with 50% argon for 30, 45 and 180 min and 30% argon for 180 min caused significant protection of A549 cells against H2O2-induced apoptosis, with increases in cellular viability of 5-47% (p < 0.0001). A small adverse effect was also observed, which presented as a 12-15% increase in cellular necrosis in argon-treated groups. Argon exposure resulted in early activation of c-Jun N-terminal kinase (JNK) and p38, peaking 10- 30 min after the start of preconditioning, and delayed activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, peaking after 60-90 min.
CONCLUSIONS: Argon preconditioning protects airway epithelial cells from H2O2-induced apoptotic cell death. Argon activates the JNK, p38, and ERK1/2 pathways, but not the Akt pathway. The cytoprotective properties of argon suggest possible prophylactic applications in surgery-related IR injury of the lungs.
© 2016 S. Karger AG, Basel.

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Year:  2016        PMID: 27560977     DOI: 10.1159/000448682

Source DB:  PubMed          Journal:  Eur Surg Res        ISSN: 0014-312X            Impact factor:   1.745


  6 in total

1.  Argon Inhalation for 24 Hours After Onset of Permanent Focal Cerebral Ischemia in Rats Provides Neuroprotection and Improves Neurologic Outcome.

Authors:  Shuang Ma; Dongmei Chu; Litao Li; Jennifer A Creed; Yu-Mi Ryang; Huaxin Sheng; Wei Yang; David S Warner; Dennis A Turner; Ulrike Hoffmann
Journal:  Crit Care Med       Date:  2019-08       Impact factor: 7.598

2.  Argon Inhalation for 24 h After Closed-Head Injury Does not Improve Recovery, Neuroinflammation, or Neurologic Outcome in Mice.

Authors:  Jennifer Creed; Viviana Cantillana-Riquelme; Bai Hui Yan; Shuang Ma; Dongmei Chu; Haichen Wang; Dennis A Turner; Daniel T Laskowitz; Ulrike Hoffmann
Journal:  Neurocrit Care       Date:  2020-09-21       Impact factor: 3.210

3.  Intermittent Hypoxia Activates Duration-Dependent Protective and Injurious Mechanisms in Mouse Lung Endothelial Cells.

Authors:  Peter Wohlrab; Lourdes Soto-Gonzales; Thomas Benesch; Max Paul Winter; Irene Marthe Lang; Klaus Markstaller; Verena Tretter; Klaus Ulrich Klein
Journal:  Front Physiol       Date:  2018-12-06       Impact factor: 4.566

Review 4.  A complete review of preclinical and clinical uses of the noble gas argon: Evidence of safety and protection.

Authors:  Francesca Nespoli; Simone Redaelli; Laura Ruggeri; Francesca Fumagalli; Davide Olivari; Giuseppe Ristagno
Journal:  Ann Card Anaesth       Date:  2019 Apr-Jun

5.  Oxygen conditions oscillating between hypoxia and hyperoxia induce different effects in the pulmonary endothelium compared to constant oxygen conditions.

Authors:  Peter Wohlrab; Michael Johann Danhofer; Wolfgang Schaubmayr; Akos Tiboldi; Katharina Krenn; Klaus Markstaller; Roman Ullrich; Klaus Ulrich Klein; Verena Tretter
Journal:  Physiol Rep       Date:  2021-02

6.  Argon inhibits reactive oxygen species oxidative stress via the miR-21-mediated PDCD4/PTEN pathway to prevent myocardial ischemia/reperfusion injury.

Authors:  Hong Qi; Jiancheng Zhang; You Shang; Shiying Yuan; Chunqing Meng
Journal:  Bioengineered       Date:  2021-12       Impact factor: 3.269

  6 in total

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