Neuroprotection (and lack of neuroprotection) afforded by a series of noble gases in an in vitro model of neuronal injury

Jawad, Noorulhuda; Rizvi, Maleeha; Gu, Jianteng; Adeyi, Olar; Tao, Guocai; Maze, Mervyn; Ma, Daqing

doi:10.1016/j.neulet.2009.05.069

Cited by 101 publications

(96 citation statements)

References 28 publications

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“…In previous studies helium has been shown to be protective in brain slices (12) and middle cerebral artery occlusion animal model (13); however we observed that helium had a detrimental effect on oxygen-glucose deprivation injury in cell culture (11). Herein helium significantly improved morphology and neurologic function from 90 minutes of hypoxic-ischemia in line with a number of previous studies (12,13,24,25) however this protection was lost against the more severe insult of 120 minutes of hypoxic-ischemia.…”

Section: Discussionsupporting

confidence: 89%

“…Argon has also been shown to exert significant neuroprotective effect in in vitro models of injury and in an adult model of hypoxic-ischemic injury in vivo (11,14). As far as we are aware this is the first report describing argon neuroprotection against hypoxic-ischemic injury in young animals.…”

Section: Discussionmentioning

confidence: 83%

“…Similar to xenon, argon and helium have shown neuroprotective qualities in vitro (11)(12)(13)(14) and in vivo (13,19) while other members of noble gas family, neon and krypton, lack effect (11). Interestingly helium has also been reported to exhibit both detrimental as well as protective effects (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

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The protective profile of argon, helium, and xenon in a model of neonatal asphyxia in rats*

Zhuang

Yang

Zhao

et al. 2012

Critical Care Medicine

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Abstract:OBJECTIVE: Xenon provides neuroprotection in multiple animal models however little is known about the other noble gases. The aim of the current study was to compare xenon, argon and helium neuroprotection in a neonatal asphyxia model in MEASUREMENTS AND MAIN RESULTS: Control animals undergoing moderatehypoxic-ischemia endured reduced neuronal survival at 7 days with impaired neurological function at the juvenile age compared with naïve animals. Severe hypoxic-ischemic damage produced a large cerebral infarction in controls. Following moderate hypoxic-ischemia, all three noble gases improved cell survival, brain structural integrity and neurological function on post-natal day 40 compared to nitrogen. Interestingly argon improved cell survival to naïve levels while xenon and helium did not. When tested against more severe hypoxic-ischemic injury only, argon and xenon reduced infarct volume. Furthermore post-injury body weight in moderate insult was lower in the helium treated group compared to the naïve, control and other noble gas treatment groups while in severe injurious setting it is lower in both control and helium treated group than other groups. In the non-directly injured hemisphere argon, helium and xenon increased the expression of Bcl-2 while helium 4 and xenon increased Bcl-xL. In addition, Bax expression was enhanced in the control and helium groups.CONCLUSIONS: These studies indicate that argon and xenon provide neuroprotection against both moderate and severe hypoxia-ischemic brain injury likely via prosurvival proteins synthesis.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 83%

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The protective profile of argon, helium, and xenon in a model of neonatal asphyxia in rats*

Zhuang

Yang

Zhao

et al. 2012

Critical Care Medicine

Self Cite

125

130

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“…Although noble gases are chemically inert, they are capable of forming induced dipole, which is attracted to the charge that induced it, or instantaneous dipole, which produces and binds to an induced dipole in a second molecule 24 . Thus, they might produce biological effects by stabilising receptors or enzymes in active or inactive forms via interactions with amino acids at the binding sites 25 .…”

Section: Discussionmentioning

confidence: 99%

Heme Oxygenase-1 Mediates Neuroprotection Conferred by Argon in Combination with Hypothermia in Neonatal Hypoxia–Ischemia Brain Injury

et al. 2016

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Background Hypoxic–ischemic encephalopathy is a major cause of mortality and disability in the newborn. The authors investigated the protective effects of argon combined with hypothermia on neonatal rat hypoxic–ischemic brain injury. Methods In in vitro studies, rat cortical neuronal cell cultures were challenged by oxygen and glucose deprivation for 90 min and exposed to 70% Ar or N2 with 5% CO2 balanced with O2, at 33°C for 2 h. Neuronal phospho-Akt, heme oxygenase-1 and phospho-glycogen synthase kinase-3β expression, and cell death were assessed. In in vivo studies, neonatal rats were subjected to unilateral common carotid artery ligation followed by hypoxia (8% O2 balanced with N2 and CO2) for 90 min. They were exposed to 70% Ar or N2 balanced with oxygen at 33°, 35°, and 37°C for 2 h. Brain injury was assessed at 24 h or 4 weeks after treatment. Results In in vitro studies, argon–hypothermia treatment increased phospho-Akt and heme oxygenase-1 expression and significantly reduced the phospho-glycogen synthase kinase-3β Tyr-216 expression, cytochrome C release, and cell death in oxygen–glucose deprivation–exposed cortical neurons. In in vivo studies, argon–hypothermia treatment decreased hypoxia/ischemia-induced brain infarct size (n = 10) and both caspase-3 and nuclear factor-κB activation in the cortex and hippocampus. It also reduced hippocampal astrocyte activation and proliferation. Inhibition of phosphoinositide-3-kinase (PI3K)/Akt pathway through LY294002 attenuated cerebral protection conferred by argon–hypothermia treatment (n = 8). Conclusion Argon combined with hypothermia provides neuroprotection against cerebral hypoxia–ischemia damage in neonatal rats, which could serve as a new therapeutic strategy against hypoxic–ischemic encephalopathy.

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“…Argon exposure before 30 min of left anterior descending coronary artery occlusion can provide myocardial protection by activating prosurvival MAPKs and inhibiting opening of mitochondrial transition pore [26]. Argon can also protect cultured neurons from 90 min of oxygen/glucose deprivation [27]. However, Rizvi et al [28] reported no protective effect of 75% argon preconditioning on oxygen/glucose deprivation injury in human tubular kidney cells, whereas 75% xenon was effective.…”

Section: Discussionmentioning

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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Neuroprotection (and lack of neuroprotection) afforded by a series of noble gases in an in vitro model of neuronal injury

Cited by 101 publications

References 28 publications

The protective profile of argon, helium, and xenon in a model of neonatal asphyxia in rats*

The protective profile of argon, helium, and xenon in a model of neonatal asphyxia in rats*

Heme Oxygenase-1 Mediates Neuroprotection Conferred by Argon in Combination with Hypothermia in Neonatal Hypoxia–Ischemia Brain Injury

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

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