Potential application value of xenon in stroke treatment

Zhao, Chongshun; Li, Hao; Wang, Zhong; Chen, Gang

doi:10.4103/2045-9912.241077

Cited by 14 publications

(4 citation statements)

References 69 publications

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“…Besides, some evidence suggests that xenon inhibits transmission and uptake of glutamate as well as further inhibit NMDA receptors through binding at the interface of NR1 and NR2 subunits (Dickinson et al, 2007;Liu et al, 2010;Zhang et al, 2021). Recently, TREK-1 gene was found to be activated by xenon, which is considered to be associated with the activation of Ca 2+ channels, reduction of glutamate release and inhibition of excitotoxicity (Zhao et al, 2018). A steadily accumulating body of evidence shows that xenon can decrease the level of glutamate, antagonize NMDA receptors, and attenuate neuroexcitotoxicity-induced oxidative stress (Lavaur et al, 2016;Zhang et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

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%

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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“…The review identified six studies that quantified the expression of B-cell lymphoma protein (Bcl-2), a pro-survival protein, following xenon exposure. The result of all six studies reported that xenon administration was associated with an increase in expression of Bcl-2 (Ma et al, 2006;Shu et al, 2010;Zhuang et al, 2012;Yang et al, 2014;Zhao et al, 2018;Jin et al, 2021).…”

Section: Downstream Proteins Involved In Cell Survival Signalingmentioning

confidence: 99%

The cellular mechanisms associated with the anesthetic and neuroprotective properties of xenon: a systematic review of the preclinical literature

McGuigan,

Marie,

O'Bryan

et al. 2023

Front. Neurosci.

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IntroductionXenon exhibits significant neuroprotection against a wide range of neurological insults in animal models. However, clinical evidence that xenon improves outcomes in human studies of neurological injury remains elusive. Previous reviews of xenon's method of action have not been performed in a systematic manner. The aim of this review is to provide a comprehensive summary of the evidence underlying the cellular interactions responsible for two phenomena associated with xenon administration: anesthesia and neuroprotection.MethodsA systematic review of the preclinical literature was carried out according to the PRISMA guidelines and a review protocol was registered with PROSPERO. The review included both in vitro models of the central nervous system and mammalian in vivo studies. The search was performed on 27th May 2022 in the following databases: Ovid Medline, Ovid Embase, Ovid Emcare, APA PsycInfo, and Web of Science. A risk of bias assessment was performed utilizing the Office of Health Assessment and Translation tool. Given the heterogeneity of the outcome data, a narrative synthesis was performed.ResultsThe review identified 69 articles describing 638 individual experiments in which a hypothesis was tested regarding the interaction of xenon with cellular targets including: membrane bound proteins, intracellular signaling cascades and transcription factors. Xenon has both common and subtype specific interactions with ionotropic glutamate receptors. Xenon also influences the release of inhibitory neurotransmitters and influences multiple other ligand gated and non-ligand gated membrane bound proteins. The review identified several intracellular signaling pathways and gene transcription factors that are influenced by xenon administration and might contribute to anesthesia and neuroprotection.DiscussionThe nature of xenon NMDA receptor antagonism, and its range of additional cellular targets, distinguishes it from other NMDA antagonists such as ketamine and nitrous oxide. This is reflected in the distinct behavioral and electrophysiological characteristics of xenon. Xenon influences multiple overlapping cellular processes, both at the cell membrane and within the cell, that promote cell survival. It is hoped that identification of the underlying cellular targets of xenon might aid the development of potential therapeutics for neurological injury and improve the clinical utilization of xenon.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, identifier: 336871.

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“…Xenon activates and opens the TREK-1 channel. Consequently, the activation of voltage-gated Ca 2+ channels on the presynaptic membrane is inhibited, glutamate release is reduced, and excitotoxicity is further inhibited (Zhao et al, 2018) (Figure 1). The above mechanism may contribute to xenon-induced neuroprotection in cerebral ischemia, stroke, and epilepsy (Mathie & Veale, 2007;Zhao et al, 2018).…”

Section: Xenon Activates the Two-pore-domain Background K + Channel Trek-1mentioning

confidence: 99%

“…Consequently, the activation of voltage-gated Ca 2+ channels on the presynaptic membrane is inhibited, glutamate release is reduced, and excitotoxicity is further inhibited (Zhao et al, 2018) (Figure 1). The above mechanism may contribute to xenon-induced neuroprotection in cerebral ischemia, stroke, and epilepsy (Mathie & Veale, 2007;Zhao et al, 2018). Bantel et al (2010) revealed that activation of the ATP-sensitive K + (K ATP ) channel plays an important role in neuroprotection and participates in the possible mechanisms of xenon-mediated neuroprotection in a stroke model.…”

Section: Xenon Activates the Two-pore-domain Background K + Channel Trek-1mentioning

confidence: 99%

The neuroprotective effect and possible therapeutic application of xenon in neurological diseases

Zhang

Cui

Cheng

et al. 2021

J of Neuroscience Research

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Xenon is an inert gas with stable chemical properties which is used as an anesthetic.Recent in vitro and in vivo findings indicate that xenon also elicits an excellent neuroprotective effect in subanesthetic concentrations. The mechanisms underlying this primarily involve the attenuation of excitotoxicity and the inhibition of N-methyldaspartic acid (NMDA) receptors and NMDA receptor-related effects, such as antioxidative effects, reduced activation of microglia, and Ca 2+ -dependent mechanisms, as well as the interaction with certain ion channels and glial cells. Based on this strong neuroprotective role, a large number of experimental and clinical studies have confirmed the significant therapeutic effect of xenon in the treatment of neurological diseases. This review summarizes the reported neuroprotective mechanisms of xenon and discusses its possible therapeutic application in the treatment of various neurological diseases.

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Potential application value of xenon in stroke treatment

Cited by 14 publications

References 69 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

The cellular mechanisms associated with the anesthetic and neuroprotective properties of xenon: a systematic review of the preclinical literature

The neuroprotective effect and possible therapeutic application of xenon in neurological diseases

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