Table 2 A Summary of the Neuroprotective Effects of Xenon
From: Application of medical gases in the field of neurobiology
Model | Intervention | Results | Reference |
|---|---|---|---|
NMDA, glutamate, or oxygen deprivation induced neuronal injury | Xenon saturated medium for 24 h (in vitro) 20%, 40%, 60%, 75% xenon (in vivo) | Xenon (60% atm) reduces LDH release to baseline with oxygen deprivation; xenon (75% atm) reduces LDH release by 80% with either NMDA-or glutamate-induced injury. In vivo, xenon exerts a concentration-dependent protective effect and reduces injury by 45% at the highest xenon concentration tested (75% atm). | [170] |
Hypoxia damaged cortical neurons from rat embryos | Xenon saturated medium for 2 h | Complete protection against cellular damage and prevention of hypoxia-induced glutamate release | [171] |
Hypoxia damaged PC-12 cells | Xenon saturated medium for up to120 min | Xenon results in complete protection against cellular damage and prevention of hypoxia-induced dopamine release in which intracellular Ca2+-ions evolve. | [172] |
MCAO in mice | 70%, 35% xenon during occlusion for 60 min | Xenon administration improves both functional and histological outcome | [173] |
Neonatal HI | 70%, 50% xenon immediately after insult for 3 h | Xenon administration commenced after hypoxia-ischemia in neonatal rats provides short-term neuroprotection | [174] |
brain slices from rats (OGD) MCAO | 15-75% xenon bubbled medium 50% xenon 2~3 h after MCAO | Xenon, administered at subanesthetic doses, offers global neuroprotection from reduction of neurotransmitter release induced by ischemia, reduces subsequent cell injury and neuronal death | [175] |
NMA induced neuronal damage | 70% xenon for 10 min at 3 h, 1, 2, 5, or 7 days before insult | Xenon alone does not induce changes, but reduces about 50% NMDA-induced cell loss as well as degenerating neurons, with the maximal neuroprotection at 7 days. | [176] |
anesthetic-induced neuronal apoptosis in vivo and in vitro | 75%, 60%, 30% xenon for 6 h | Xenon attenuates isoflurane-induced apoptosis. | [164] |
nitrous oxide and isoflurane induced damage | 70% xenon for 2 h | Xenon pre-treatment prevents nitrous oxide-and isoflurane-induced neuroapoptosis (in vivo and in vitro) and cognitive deterioration (in vivo) | [165] |
OGD induced damage to neurons from neonatal mice | 75% xenon + Dex (0.001~10 μM) for 6 h | Combination of Xenon and Dex offers neuroprotection additively in vitro and synergistically in vivo | [178] |
neonatal HI | 20-70% xenon for 90 min during hypoxia or 2, 24 h after hypoxia + hypothermia (30-37°C) | Xenon and hypothermia administered 4 h after hypoxic-ischemic injury in neonatal rats provides synergistic neuroprotection | [177] |
OGD induced damage to neurons; neonatal HI | 25~75% xenon for 120 min (in vitro); 70% xenon for 120 min (in vivo) | Prosurvival proteins Bcl-2 and brain-derived neurotrophic factor are upregulated by xenon treatment | [179] |
OGD induced damage to neurons; neonatal HI | 12.5~75% xenon for 2 h (in vitro); 20%, 75% for 2 h (in vivo) | Pre-conditioning with xenon and the combination of xenon and sevoflurane results in long-term functional neuroprotection associated with enhanced phosphorylated cyclic adenosine monophosphate response element binding protein signaling | [180] |
MCAO in mice | 70% xenon for 2 h | Xenon pre-conditioning improves histological and neurological functional outcome in both genders in a stroke model of mice in which HIF-1α and phosphoAkt evolve | [207] |
OGD induced damage to neurons | 75% xenon for 2 h | Xenon pre-conditioning clearly involves the activation of KATP channels. | [208] |