PMID- 36453425
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230116
IS  - 1673-5374 (Print)
IS  - 1876-7958 (Electronic)
IS  - 1673-5374 (Linking)
VI  - 18
IP  - 6
DP  - 2023 Jun
TI  - Argon preconditioning protects neuronal cells with a Toll-like receptor-mediated 
      effect.
PG  - 1371-1377
LID - 10.4103/1673-5374.355978 [doi]
AB  - The noble gas argon has the potential to protect neuronal cells from cell death. 
      So far, this effect has been studied in treatment after acute damage. 
      Preconditioning using argon has not yet been investigated. In this study, human 
      neuroblastoma SH-SY5Y cells were treated with different concentrations of argon 
      (25%, 50%, and 74%; 21% O(2), 5% CO(2), balance nitrogen) at different time 
      intervals before inflicting damage with rotenone (20 microM, 4 hours). Apoptosis was 
      determined by flow cytometry after annexin V and propidium iodide staining. 
      Surface expressions of Toll-like receptors 2 and 4 were also examined. Cells were 
      also processed for analysis by western blot and qPCR to determine the expression 
      of apoptotic and inflammatory proteins, such as extracellular-signal regulated 
      kinase (ERK1/2), nuclear transcription factor-kappaB (NF-kappaB), protein kinase B (Akt), 
      caspase-3, Bax, Bcl-2, interleukin-8, and heat shock proteins. 
      Immunohistochemical staining was performed for TLR2 and 4 and interleukin-8. 
      Cells were also pretreated with OxPAPC, an antagonist of TLR2 and 4 to elucidate 
      the molecular mechanism. Results showed that argon preconditioning before 
      rotenone application caused a dose-dependent but not a time-dependent reduction 
      in the number of apoptotic cells. Preconditioning with 74% argon for 2 hours was 
      used for further experiments showing the most promising results. Argon decreased 
      the surface expression of TLR2 and 4, whereas OxPAPC treatment partially 
      abolished the protective effect of argon. Argon increased phosphorylation of 
      ERK1/2 but decreased NF-kappaB and Akt. Preconditioning inhibited mitochondrial 
      apoptosis and the heat shock response. Argon also suppressed the expression of 
      the pro-inflammatory cytokine interleukin-8. Immunohistochemistry confirmed the 
      alteration of TLRs and interleukin-8. OxPAPC reversed the argon effect on ERK1/2, 
      Bax, Bcl-2, caspase-3, and interleukin-8 expression, but not on NF-kappaB and the 
      heat shock proteins. Taken together, argon preconditioning protects against 
      apoptosis of neuronal cells and mediates its action via Toll-like receptors. 
      Argon may represent a promising therapeutic alternative in various clinical 
      settings, such as the treatment of stroke.
FAU - Scheid, Stefanie
AU  - Scheid S
AD  - Department of Anesthesiology and Critical Care, Medical Center - University of 
      Freiburg, Faculty of Medicine, Freiburg, Germany.
FAU - Lejarre, Adrien
AU  - Lejarre A
AD  - Department of Anesthesiology and Critical Care, Medical Center - University of 
      Freiburg, Faculty of Medicine, Freiburg, Germany.
FAU - Wollborn, Jakob
AU  - Wollborn J
AD  - Department of Anesthesiology and Critical Care, Medical Center - University of 
      Freiburg, Faculty of Medicine, Freiburg, Germany; Department of Anesthesiology, 
      Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical 
      School, Boston, MA, USA.
FAU - Buerkle, Hartmut
AU  - Buerkle H
AD  - Department of Anesthesiology and Critical Care, Medical Center - University of 
      Freiburg, Faculty of Medicine, Freiburg, Germany.
FAU - Goebel, Ulrich
AU  - Goebel U
AD  - Department of Anesthesiology and Critical Care Medicine, St. Franziskus-Hospital, 
      Muenster, Germany.
FAU - Ulbrich, Felix
AU  - Ulbrich F
AD  - Department of Anesthesiology and Critical Care, Medical Center - University of 
      Freiburg, Faculty of Medicine, Freiburg, Germany.
LA  - eng
PT  - Journal Article
PL  - India
TA  - Neural Regen Res
JT  - Neural regeneration research
JID - 101316351
PMC - PMC9838174
OTO - NOTNLM
OT  - SH-SY5Y
OT  - Toll-like receptor 2
OT  - Toll-like receptor 4
OT  - apoptosis
OT  - inflammation
OT  - interleukin-8
OT  - neuroprotection
OT  - rotenone
COIS- None
EDAT- 2022/12/02 06:00
MHDA- 2022/12/02 06:01
PMCR- 2022/10/11
CRDT- 2022/12/01 05:07
PHST- 2022/12/01 05:07 [entrez]
PHST- 2022/12/02 06:00 [pubmed]
PHST- 2022/12/02 06:01 [medline]
PHST- 2022/10/11 00:00 [pmc-release]
AID - NeuralRegenRes_2023_18_6_1371_355978 [pii]
AID - NRR-18-1371 [pii]
AID - 10.4103/1673-5374.355978 [doi]
PST - ppublish
SO  - Neural Regen Res. 2023 Jun;18(6):1371-1377. doi: 10.4103/1673-5374.355978.