European Surgical Research
Original Paper
Argon Preconditioning Protects Airway Epithelial Cells against Hydrogen Peroxide-Induced Oxidative StressHafner C.a · Qi H.a, b · Soto-Gonzalez L.a · Doerr K.c · Ullrich R.a · Tretter E.V.a · Markstaller K.a · Klein K.U.aaDepartment of Anaesthesia, General Intensive Care and Pain Management, Medical University of Vienna, Vienna, Austria; bDepartment of Anaesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; cDepartment of Internal Medicine III, Medical University of Vienna, Vienna, Austria
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Article / Publication Details
Received: February 07, 2016
Accepted: July 25, 2016
Published online: August 25, 2016
Issue release date: November 2016
Number of Print Pages: 11
Number of Figures: 5
Number of Tables: 0
ISSN: 0014-312X (Print)
eISSN: 1421-9921 (Online)
For additional information: https://www.karger.com/ESR
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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Article / Publication Details
Received: February 07, 2016
Accepted: July 25, 2016
Published online: August 25, 2016
Issue release date: November 2016
Number of Print Pages: 11
Number of Figures: 5
Number of Tables: 0
ISSN: 0014-312X (Print)
eISSN: 1421-9921 (Online)
For additional information: https://www.karger.com/ESR
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