Xenon

Korsunsky, Galina

doi:10.1097/aia.0000000000000049

Cited by 2 publications

(5 citation statements)

References 60 publications

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“…Xenon is an ideal anesthetic with excellent safety characteristics ( Korsunsky, 2015 ). In the past 50 years, the safety of xenon has been strongly established in clinical settings ( Wilhelm et al, 2002 ).…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Xenon, a colorless and odorless monoatomic noble gas, was discovered in 1898 and first used as an anesthetic in 1951 ( Korsunsky, 2015 ). Xenon is non-flammable, non-explosive, non-toxic, and non-teratogenic ( Korsunsky, 2015 ). Moreover, xenon cannot be metabolized and is discharged through the lungs rather than the liver or kidney, rendering it the preferred treatment for patients with impaired liver and kidney function ( Maze and Laitio, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

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Xenon inhalation attenuates neuronal injury and prevents epilepsy in febrile seizure Sprague-Dawley pups

Cheng,

Zhai,

Yuan

et al. 2023

Front. Cell. Neurosci.

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BackgroundFebrile seizures (FS) usually occur in childhood and may cause irreversible neuronal damage, cognitive functional defects, and an increase in the risk of epilepsy later in life. Anti-epileptic drugs (AEDs), currently used to treat FS in children, can relieve seizures. However, their effects in preventing the risk of developing epilepsy in later life are unsatisfactory. Moreover, AEDs may damage child brain development. Here, we evaluated the efficiency of xenon in treating prolonged FS (PFS) and preventing epilepsy in Sprague-Dawley pups.MethodsProlonged FS was induced by hyperthermic treatment. After 90 min of PFS, the pups in the xenon treatment group were immediately treated with 70% xenon/21% oxygen/9% nitrogen for 60 min. The levels of glutamate, mitochondrial oxidative stress, mitophagy, and neuronal injury, seizures, learning, and memory functions were measured at specific time points.ResultsNeonatal period PFS led to spontaneous seizure, learning and memory dysfunction, accompanied by increased levels of glutamate, mitochondrial oxidative stress, mitophagy, and neuronal injury. Xenon treatment alleviated the changes caused by PFS and reduced the risk of PFS developing into epilepsy later.ConclusionOur results suggest that xenon inhalation could be a potential therapeutic strategy to attenuate neuronal injury and prevent epilepsy in patients with FS.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Xenon inhalation attenuates neuronal injury and prevents epilepsy in febrile seizure Sprague-Dawley pups

Cheng,

Zhai,

Yuan

et al. 2023

Front. Cell. Neurosci.

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“…However, due to the particularity of neonatal medication, treatment of HIBD currently remains a challenge. Application of Xe may be advantageous in the treatment of HIBD as Xe has the characteristics of low toxicity, easy to dissolve in the blood, convenient and quick inhalation and administration, and fast excretion, which makes it safe for newborns to use [9]. Actually, Xe has been used in the clinic for about 70 years [21].…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, inhibition of autophagy may be a promising therapeutic strategy for mitigating the degrees of HIBD in neonatal mice. Xenon (Xe) is an inert, colorless, odorless, heavy gas, and was discovered in 1898 [9]. Previous studies have reported that Xe at a subanesthetic concentration can protect from neuronal damage caused by cerebral ischemia, spinal cord ischemia and traumatic brain injury [10], and improve surgery-related cognitive impairment in elderly patients [11].…”

Section: Introductionmentioning

confidence: 99%

Xenon attenuates hypoxic-ischemic brain damage by inhibiting autophagy in neonatal rats

Sun

Wei

et al. 2023

NeuroReport

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Xenon (Xe) is an inert, colorless and odorless heavy gas and has many biological functions. However, little is known about whether and how Xe can modulate hypoxic-ischemic brain damage (HIBD) in neonatal rats. This study employed a neonatal rat model to explore the potential effect of Xe on neuron autophagy and the severity of HIBD. Neonatal Sprague–Dawley rats were subjected to HIBD, randomized and treated with Xe or mild hypothermia (at 32 °C) for 3 h. The degrees of HIBD, neuron autophagy and the neuronal functions in some neonates from each group were tested by histopathology, immunochemistry, transmission electron microscopy, western blot, open-field and Trapeze tests at 3 and 28 days post-induction of HIBD, respectively. Compared with the Sham group, hypoxic-ischemia caused larger volumes of cerebral infarction and severe brain damage, and increased autophagosome formation and Beclin-1 and microtubule-associated protein 1A/1B-light chain 3 class II (LC3-II) expression in the brain of rats, accompanied by the defect in neuronal functions. In contrast, treatment with Xe and/or hypothermia significantly reduced infarct volumes and ameliorated neurological defects in the HIBD rats, particularly for the combination of Xe and hypothermia. Xe significantly mitigated the relative levels of Beclin-1 and LC3-II expression and autophagosome formation induced by HIBD in rats. Xe acted as a neuroprotective factor against HIBD, possibly by inhibiting the hypoxia-induced neuron autophagy in rats.

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Xenon

Cited by 2 publications

References 60 publications

Xenon inhalation attenuates neuronal injury and prevents epilepsy in febrile seizure Sprague-Dawley pups

Xenon inhalation attenuates neuronal injury and prevents epilepsy in febrile seizure Sprague-Dawley pups

Xenon attenuates hypoxic-ischemic brain damage by inhibiting autophagy in neonatal rats

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