The Neuroprotective Effect of Xenon Administration during Transient Middle Cerebral Artery Occlusion in Mice

Homi, H. Mayumi; Yokoo, Noriko; Ma, Daqing; Warner, David S.; Franks, Nicholas P.; Maze, Mervyn; Grocott, Hilary P.

doi:10.1097/00000542-200310000-00020

Cited by 162 publications

(113 citation statements)

References 26 publications

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“…In addition, post-injury treatment with xenon 2 hours after a HI insult was also shown to be neuroprotective; again this effect was most marked in the CA1 region of the hippocampus. The neuroprotection afforded by xenon preconditioning and post-injury treatment in the organotypic hippocampal slice model, corroborated previous data from a variety of other in vivo and in vitro studies (18)(19)(20)(21), hence validating the use of this model for further studies of xenon neuroprotection.…”

Section: Discussionsupporting

confidence: 84%

“…Xenon, an NMDA receptor antagonist, has been shown to be neuroprotective in several paradigms of neuronal injury in both in vitro and in vivo models (18)(19)(20)(21). In vitro models, it offers the ability to strictly control the microenvironment and easily quantify cell death; however the major disadvantage is a loss of synaptic connections.…”

Section: Discussionmentioning

confidence: 99%

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Xenon Confers Neuroprotection in Organotypic Hippocampal Slice Cultures

Lan¹,

Sodha²,

Wang³

et al. 2016

J Anesth Perioper Med

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Background: The present study sought to establish the use of a novel model of cerebral ischaemia in which to investigate the neuroprotective effects of xenon based on organotypic hippocampal slice cultures. Methods: Organotypic hippocampal slices, derived from 7-10 days post-natal C57B16 mouse pups, were placed and cultured for 10-14 days on membranous inserts. Neuronal injury of cultures was provoked with media deprived with oxygen and glucose (OGD) for 2 hours. Cultures were exposed to 25% xenon or 50% xenon and 20% oxygen and 5% carbon dioxide (CO2) balanced with nitrogen (N2) 24 hours before OGD insult (preconditioning) for 2 hours or 75% xenon and 5% CO2 balanced with oxygen 4 hours after OGD for 2 hours. Cell death was quantified by assessment of propidium iodide (PI) uptake before and after OGD up to 72 hours in the CA1 and the dentate gyrus (DG) of the hippocampus. Results: Xenon preconditioning at concentrations of 25% and 50% resulted in a significant reduction in PI uptake in the CA1 region of the hippocampus compared with the control group (P<0.01). The effect was less pronounced in the DG region with xenon only at a concentration of 25% (P<0.05). Xenon 75% treatment 4 hours postinsult significantly attenuated cell death in both the DG and CA1 areas of the hippocampus. Conclusions: This study corroborated previous data to confirm that xenon is a potent neuroprotectant, and advocated its potential for future use in specific clinical settings.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Xenon Confers Neuroprotection in Organotypic Hippocampal Slice Cultures

Lan¹,

Sodha²,

Wang³

et al. 2016

J Anesth Perioper Med

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“…The decision to explore this with the noble anaesthetic gas xenon is predicated by its very rapid onset and recovery characteristics, its lack of side effects Sanders et al, 2005) and the recent demonstration of its neuroprotective potential in both in vitro and in vivo models of acute neuronal injury (Ma et al, , 2003aWilhelm et al, 2002;Petzelt et al, 2003;Homi et al, 2003). Thus, we have investigated whether xenon is capable of preconditioning using a series of models from an in vitro glial-neuronal cell coculture system, through a hippocampal slice culture preparation, to an in vivo neonatal rat model.…”

Section: Introductionmentioning

confidence: 99%

Xenon Preconditioning Reduces Brain Damage from Neonatal Asphyxia in Rats

Hossain

Pettet

et al. 2006

J Cereb Blood Flow Metab

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166

111

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Xenon attenuates on-going neuronal injury in both in vitro and in vivo models of hypoxic-ischaemic injury when administered during and after the insult. In the present study, we sought to investigate whether the neuroprotective efficacy of xenon can be observed when administered before an insult, referred to as 'preconditioning'. In a neuronal-glial cell coculture, preexposure to xenon for 2 h caused a concentration-dependent reduction of lactate dehydrogenase release from cells deprived of oxygen and glucose 24 h later; xenon's preconditioning effect was abolished by cycloheximide, a protein synthesis inhibitor. Preconditioning with xenon decreased propidium iodide staining in a hippocampal slice culture model subjected to oxygen and glucose deprivation. In an in vivo model of neonatal asphyxia involving hypoxic-ischaemic injury to 7-day-old rats, preconditioning with xenon reduced infarction size when assessed 7 days after injury. Furthermore, a sustained improvement in neurologic function was also evident 30 days after injury. Phosphorylated cAMP (cyclic adenosine 3 0 ,5 0 -monophosphate)-response element binding protein (pCREB) was increased by xenon exposure. Also, the prosurvival proteins Bcl-2 and brain-derived neurotrophic factor were upregulated by xenon treatment. These studies provide evidence for xenon's preconditioning effect, which might be caused by a pCREB-regulated synthesis of proteins that promote survival against neuronal injury.

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“…The inert anesthetic gas xenon has received increasing interest as a neuroprotectant over the last decade. Xenon has proven to be neuroprotective both in vivo and in vitro with minimal adverse effects (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21). We and others have previously reported that adding immediate xenon to HT enhanced the neuroprotective effects of HT after induced hypoxia-ischemia in neonatal rats (12,13,15,20) and newborn pigs (21).…”

mentioning

confidence: 95%