ArticleNeurocritical care2022
Timely and Appropriate Administration of Inhaled Argon Provides Better Outcomes for tMCAO Mice: A Controlled, Randomized, and Double-Blind Animal Study.
Article in Neurocritical care, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Neuroprotective effects of noble gases following acquired brain injury: a narrative review.Frontiers in pharmacology · 2026Review
- Therapeutic Effects of Argon Inhalation on Lung Ischemia-Reperfusion Injury in CLAWN Miniature Swine.Journal of clinical medicine · 2025Article
- Argon improves microglia-mediated hippocampal neuronal hyperexcitability to alleviate anxiety-like behaviors in mice.Journal of molecular cell biology · 2025Article
- Argon mitigates post-stroke neuroinflammation by regulating M1/M2 polarization and inhibiting NF-κB/NLRP3 inflammasome signaling.Journal of molecular cell biology · 2023Article
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10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInhaled argon (iAr) has shown promising therapeutic efficacy for acute ischemic stroke and has exhibited impressive advantages over other inert gases as a neuroprotective agent. However, the optimal dose, duration, and time point of iAr for acute ischemic stroke are unknown. Here, we explored variable iAr schedules and evaluated the neuroprotective effects of acute iAr administration on lesion volume, brain edema, and neurological function in a mouse model of cerebral ischemic/reperfusion injury.
methodsAdult ICR (Institute of Cancer Research) mice were randomly subjected to sham, moderate (1.5 h), or severe (3 h) transient middle cerebral artery occlusion (tMCAO). One hour after tMCAO, the mice were randomized to variable iAr protocols or air. General and focal deficit scores were assessed during double-blind treatment. Infarct volume, overall recovery, and brain edema were analyzed 24 h after cerebral ischemic/reperfusion injury.
resultsCompared with those in the tMCAO-only group, lesion volume (p < 0.0001) and neurologic outcome (general, p < 0.0001; focal, p < 0.0001) were significantly improved in the group administered iAr 1 h after stroke onset (during ischemia). Short-term argon treatment (1 or 3 h) significantly improved the infarct volume (1 vs. 24 h, p < 0.0001; 3 vs. 24 h, p < 0.0001) compared with argon inhalation for 24 h. The concentration of iAr was confirmed to be a key factor in improving focal neurological outcomes relative to that in the tMCAO group, with higher concentrations of iAr showing better effects. Additionally, even though ischemia research has shown an increase in cerebral damage proportional to the ischemia time, argon administration showed significant neuroprotective effects on infarct volume (p < 0.0001), neurological deficits (general, p < 0.0001; focal, p < 0.0001), weight recovery (p < 0.0001), and edema (p < 0.0001) in general, particularly in moderate stroke.
conclusionsTimely iAr administration during ischemia showed optimal neurological outcomes and minimal infarct volumes. Moreover, an appropriate duration of argon administration was important for better neuroprotective efficacy. These findings may provide vital guidance for using argon as a neuroprotective agent and moving to clinical trials in acute ischemic stroke.
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