Expression analysis following argon treatment in an in vivo model of transient middle cerebral artery occlusion in rats

Fahlenkamp, Astrid; Coburn, Mark; Prada, Antonio de; Gereitzig, Nadine; Beyer, Cordian; Haase, Hajo; Rossaint, Rolf; Gempt, Jens; Ryang, Yu‐Mi

doi:10.1186/2045-9912-4-11

Cited by 31 publications

(43 citation statements)

References 35 publications

(50 reference statements)

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“…In 2014, Fahlenkamp et al [24] performed 2 h of tMCAO in rats. After one hour of tMCAO, animals received argon (50% argon, 50% O 2 ) or placebo (50% N 2 , 50% O 2 ) for the next tMCAO hour via face mask.…”

Section: Argon As a Neuroprotective Gaseous Molecule In Various Momentioning

confidence: 99%

The Molecular Pathway of Argon-Mediated Neuroprotection

Ulbrich

Goebel

2016

IJMS

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The noble gas argon has attracted increasing attention in recent years, especially because of its neuroprotective properties. In a variety of models, ranging from oxygen-glucose deprivation in cell culture to complex models of mid-cerebral artery occlusion, subarachnoid hemorrhage or retinal ischemia-reperfusion injury in animals, argon administration after individual injury demonstrated favorable effects, particularly increased cell survival and even improved neuronal function. As an inert molecule, argon did not show signs of adverse effects in the in vitro and in vivo model used, while being comparably cheap and easy to apply. However, the molecular mechanism by which argon is able to exert its protective and beneficial characteristics remains unclear. Although there are many pieces missing to complete the signaling pathway throughout the cell, it is the aim of this review to summarize the known parts of the molecular pathways and to combine them to provide a clear insight into the cellular pathway, starting with the receptors that may be involved in mediating argons effects and ending with the translational response.

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Section: Argon As a Neuroprotective Gaseous Molecule In Various Momentioning

confidence: 99%

The Molecular Pathway of Argon-Mediated Neuroprotection

Ulbrich

Goebel

2016

IJMS

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“…Hence, we investigated the mRNA levels of representative genes which, especially in the first few hours after hepatectomy (“priming phase”), are of particular importance [2,21]. Additionally, a connection to the previously proven effects of argon on these genes should exist [8,13]. …”

Section: Resultsmentioning

confidence: 99%

“…In an experiment on rats, it was found that 24 h after transient middle cerebral artery occlusion there was a significant increase in IL-6 and TNF in the penumbra following 1 h of 50 vol% argon inhalation in comparison to a group with nitrogen inhalation [13]. …”

Section: Discussionmentioning

confidence: 99%

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Argon Delays Initiation of Liver Regeneration after Partial Hepatectomy in Rats

et al. 2017

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Background: The liver can heal up to restitutio ad integrum following damage resulting from various causes. Different studies have demonstrated the protective effect of argon on various cells and organs. To the best of our knowledge, the organ-protective effects of the noble gas argon on the liver have not yet been investigated, although argon appears to influence signal paths that are well-known mediators of liver regeneration. We hypothesized that argon inhalation prior to partial hepatectomy (70%) has a positive effect on the initiation of liver regeneration in rats. Methods: Partial hepatectomy (70%) with or without inhaled argon (50 vol%) was performed for 1 h. Liver tissue was harvested after 3, 36, and 96 h to analyze the mRNA and protein expression of hepatocyte growth factor (HGF), interleukin-6 (IL-6), tumor necrosis factor-α, and extracellular signal-regulated kinase 1/2. Histological tissue samples were prepared for immunohistochemistry (bromodeoxyuridine [BrdU], Ki-67, and TUNEL) and blood was analyzed regarding the effects of argon on liver function. Statistical analyses were performed using 1-way ANOVA followed by the post hoc Tukey-Kramer test. Results: After 3 h, the primary outcome parameter of hepatocyte proliferation was significantly reduced with argon 50 vol% inhalation in comparison to nitrogen inhalation (BrdU: 15.7 ± 9.7 vs. 7.7 ± 3.1 positive cells/1,000 hepatocytes, p = 0.013; Ki-67: 17.6 ± 13.3 vs. 4.7 ± 5.4 positive cells/1,000 hepatocytes, p = 0.006). This was most likely mediated by significant downregulation of HGF (after 3 h: 5.2 ± 3.2 vs. 2.3 ± 1.0 fold, p = 0.032; after 96 h: 2.1 ± 0.5 vs. 1.3 ± 0.3 fold, p = 0.029) and IL-6 (after 3 h: 43.7 ± 39.6 vs. 8.5 ± 9.2 fold, p = 0.032). Nevertheless, we could detect no significant effect on the weight of the residual liver, liver-body weight ratio, or liver blood test results after argon inhalation. Conclusion: Impairment of liver regeneration was apparent after argon 50 vol% inhalation that was most probably mediated by downregulation of HGF and IL-6 in the initial phase. However, the present study was not adequately powered to prove that argon has detrimental effects on the liver. Further studies are needed to evaluate the effects of argon on livers with preexisting conditions as well as on ischemia-reperfusion models.

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“…Rodent models of cardiac arrest followed by cardiopulmonary resuscitation have exhibited improved neurological performance and decreased neuronal damage with argon postconditioning [7,8,9]. Argon postconditioning was also neuroprotective in stroke models (middle cerebral artery occlusion) [10,11] and in vitro models of cerebral ischaemia and traumatic brain injury [12,13,14]. In vitro studies using organotypic cultures or tumour cells have demonstrated that argon treatment also protects against ultraviolet irradiation [15] and cytotoxic agents [16,17].…”

Section: Introductionmentioning

confidence: 99%

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

Hafner

Soto-Gonzalez

et al. 2016

Eur Surg Res

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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.

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Expression analysis following argon treatment in an in vivo model of transient middle cerebral artery occlusion in rats

Cited by 31 publications

References 35 publications

The Molecular Pathway of Argon-Mediated Neuroprotection

The Molecular Pathway of Argon-Mediated Neuroprotection

Argon Delays Initiation of Liver Regeneration after Partial Hepatectomy in Rats

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

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