Table 1.
Article | Cell/tissue | Model | Ar treatment | Histopathology/functionality | Biochemistry |
---|---|---|---|---|---|
Lemoine et al., 2017[17] | 1. Cardiomyo cytes | H/R | Ar 70% | EAD: ↑ | NA |
Duration: 5 min | Conduction blocks: ↑ | ||||
2. Human right atrial appendage | Reentries: ↑ | ||||
Contractile force: ↑ | |||||
Mayer et al., 2016[18] | Cardiomyocytes | Hypoxia + Ar preconditioning | Ar 50% | Cell survival: ↑ | HSP27: + |
Duration: 1 h | SOD2: + | ||||
VEGF: + | |||||
iNOS: + | |||||
COX2: ≈ | |||||
STAT3: ≈ | |||||
HSPA4: ≈ | |||||
HIF1α: ≈ | |||||
ERK1-2 phosphorylation: ≈ | |||||
Akt: ≈ | |||||
Hafner et al., 2016[19] | Airway epithelial cells | N2O2 oxidative stress + Ar preconditioning | Ar 30-50% | Apoptosis: ↑ | JNK: + |
Duration: 30-180 min | Cell viability: ↑ | p38: + | |||
ERK 1-2: + | |||||
Akt: ≈ | |||||
Ulbrich et al., 2015[20] | Human neuroblastoma cells | Drug-induced cell injury (rotenone) | Ar 25-75% | Apoptosis: ↑ | TLR 2 - 4: - |
Duration: 2-4 h | IRAK 4: - | ||||
ERK1 - 2: + | |||||
Caspase-3: - | |||||
Rizvi et al., 2010[21] | Human tubular kidney cells | OGD + Ar preconditioning | Ar 75% | Cell viability: ≈ | p-AKT: ≈ |
Duration: 3 h | HIF1α: ≈ | ||||
Bcl 2: ≈ | |||||
Ulbrich et al., 2016[22] | Human neuroblastoma cells | Drug-induced cell injury (rotenone) | Ar 75% | NA | Mithocondrial ΔΨ: ↑ |
Duration: 2 h | ROS: - | ||||
NF-kB: - | |||||
STAT3: - | |||||
IL-8: - | |||||
Spaggiari et al., 2013[23] | Human osteosarcoma cells | Drug-induced cell injury (STS, MTX, rotenone, antimycin A, menadione) | Ar 75% | NA | Caspase 3: - |
Duration: 6-16 h | Cytochrome c: - | ||||
Mithocondrial ΔΨ: ↑ | |||||
Fahlenkamp et al., 2012[24] | Neuronal, astroglial cells, and microglial cells | Selective influence of | Ar 50% | NA | Phospho-ERK 1-2: + |
Ar on ERK 1-2 | Duration: 15-120 min | IL 1β: -/≈ | |||
TNFα: ≈ | |||||
IL 6: ≈ | |||||
Jawad et al., 2009[25] | Neuronal cells | OGD+hypoxia | Ar 75% | Cell viability: ↑ | Cell reducing ability: ↑ |
Duration: 24 h | |||||
Loetscher et al., 2009[26] | Hippocampal slices | 1. OGD | Ar 25-74% | OGD and TBI tissue injury: ↑ | NA |
2. TBI above CA1 | Duration: 72 h | ||||
David et al., 2012[27] | Brain coronal slices | OGD | Ar 25-75% | NA | LDH release: - |
Duration: 3 h | |||||
Zhao et al., 2016[28] | Rat cortical neuronal cultures | OGD | Ar 70% + MTH | Neuronal death: ↑ | HO-1: + |
Duration: 2h | p-Akt: + | ||||
Zhao et al., 2016[29] | Rat cortical neuronal cultures | OGD | Ar 70% | Cell viability: ↑ | PI-3K: + |
Duration: 2 h | Erk 1/2: + | ||||
mTOR: + | |||||
Nrf2: + | |||||
ROS: - | |||||
Harris et al., 2013[30] | Mouse hippocampal slices | Focal mechanical trauma | Ar 33% Duration: 30 mins-24 h | Cell injury (PI): ↑ | NA |
Yarin et al., 2005[31] | Rat organ of Corti cultures | 1. Hypoxia | 1. Ar 95% | 1. Number of OHC: ↑ | NA |
Duration: 30 h | Number of IHC: ↑ | ||||
2. Drug-induced cell injury (cisplatin) | 2. and 3. Ar 74% | 2. Number of OHC: ↑ | |||
3. Drug-induced cell injury (gentamycin) | Duration: 48 h | Number of IHC: ≈ | |||
3. Number of OHC: ↑ Number of IHC: ↑ | |||||
David et al., 2013[32] | Enzymatic and thrombolytic efficiency of tPA | 1. Catalytic efficiency: | Ar 25-75% | NA | 1. Catalytic efficacy |
tPA + specific chromogenic substrate + distilled water saturated solution | Duration: 120 min | Ar 75%: + | |||
Ar 50: ≈ | |||||
Ar 25%: - | |||||
2. Thrombolytic efficiency | 2. Thrombolytic efficacy | ||||
whole blood (rats) + saline + tPA saturated solution | Ar 75%: + | ||||
Ar 50: ≈ | |||||
Ar 30%: - | |||||
Grüßer et al., 2017[33] | Hippocampal slices | TBI | Ar 50% | Cell survival≈ | NA |
Duration: 2 h |
↑: Treatment with Ar was significantly cell protective compared to control; ≈: Treatment with Ar was equivalent to control; +: Increased with Ar treatment compared to control; -: Decreased with Ar treatment compared to control, Ar: Argon, O2: Oxygen, CO2: Carbon dioxide, N2: Nitrogen, He: Helium, Kr Krypton, Xe Xenon, Ne: Neon, NA: Not available, H/R: Hypoxia-reoxygenation, EAD: Early after depolarization, HSP: Heat shock protein, SOD: Superoxide dismutase, VEGF: Vascular endothelial growth factor, iNOS: Inducible nitric oxide synthase, COX: Cyclooxygenase, STAT: Signal transducers and activator of transcription, HIF: Hypoxia-inducible factor, ERK: Extracellular signal-regulated protein kinases, p-Akt (also known as PKB): Phospho protein kinase B, N2O2: Nitrogen peroxide, JNK: c-Jun N-terminal kinase, p38: Protein 38, TLR: Toll-like receptor, IRAK: IL-1 Receptor-associated kinase, Bcl: B-cell lymphoma, OGD: Oxygen-glucose deprivation, ΔΨ: Membrane potential, ROS: Reactive oxygen species, NFkB: Nuclear factor-kB, IL: Interleukin, MTX: Mitoxantrone, STS: Broad-spectrum kinase inhibitor staurosporine, LPS: Lipopolysaccharide, TNF: Tumor necrosis factor, TBI: Traumatic brain injury, LDH: Lactate dehydrogenase, MTH: Mild therapeutic hypothermia, HO-1: Heme oxygenase-1, PI-3K: Phosphatidylinositol-3-kinases, mTOR: Mechanistic target of rapamycin, Nrf2: Nuclear factor (erythroid-derived 2) factor 2, PI: Propidium iodide, OHC: Outer hair cells, IHC: Inner hair cells, tPA: Tissue plasminogen activator