Argon mediates anti-apoptotic signaling and neuroprotection via inhibition of toll-like receptor 2 and 4

Abstract: PurposeRecently, the noble gas argon attracted significant attention due to its neuroprotective properties. However, the underlying molecular mechanism is still poorly understood. There is growing evidence that the extracellular regulated kinase 1/2 (ERK1/2) is involved in Argon´s protective effect. We hypothesized that argon mediates its protective effects via the upstream located toll-like receptors (TLRs) 2 and 4.MethodsApoptosis in a human neuroblastoma cell line (SH-SY5Y) was induced using rotenone. Argon treatment was performed after induction of apoptosis with different concentrations (25, 50 and 75 Vol% in oxygen 21 Vol%, carbon dioxide and nitrogen) for 2 or 4 hours respectively. Apoptosis was analyzed using flow cytometry (annexin-V (AV)/propidiumiodide (PI)) staining, caspase-3 activity and caspase cleavage. TLR density on the cells’ surface was analyzed using FACS and immunohistochemistry. Inhibition of TLR signaling and extracellular regulated kinase 1/2 (ERK1/2) were assessed by western blot, activity assays and FACS analysis.ResultsArgon 75 Vol% treatment abolished rotenone-induced apoptosis. This effect was attenuated dose- and time-dependently. Argon treatment was accompanied with a significant reduction of TLR2 and TLR4 receptor density and protein expression. Moreover, argon mediated increase in ERK1/2 phosphorylation was attenuated after inhibition of TLR signaling. ERK1/2 and TLR signaling inhibitors abolished the anti-apoptotic and cytoprotective effects of argon. Immunohistochemistry results strengthened these findings

Standort
Deutsche Nationalbibliothek Frankfurt am Main
Umfang
Online-Ressource
Sprache
Englisch
Anmerkungen
PLoS ONE. 10, 12 (2015), e0143887, DOI 10.1371/journal.pone.0143887, issn: 1932-6205
IN COPYRIGHT http://rightsstatements.org/page/InC/1.0 rs

Schlagwort
Apoptosis
Immunologie
Immunsystem
Lymphozyt
Leukozyt
Immunität
Resistenz
Immunchemie

Ereignis
Veröffentlichung
(wo)
Freiburg
(wer)
Universität
(wann)
2015
Urheber
Beteiligte Personen und Organisationen
Institut für Rechtsmedizin
Klinik für Anästhesiologie und Intensivmedizin
Medizinische Fakultät
Albert-Ludwigs-Universität Freiburg

DOI
10.1371/journal.pone.0143887
URN
urn:nbn:de:bsz:25-freidok-121086
Rechteinformation
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Letzte Aktualisierung
14.08.2025, 10:59 MESZ

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  • 2015

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