ArticleMetabolic brain disease2026
NREP is involved in xenon's protection against ischemic stroke injury through modulating microglial M1 polarization and neuroinflammation.
Article in Metabolic brain disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemic stroke (IS) is associated with high mortality and disability rates, and secondary neuroinflammation is a key driver of exacerbated neuronal damage. Xenon (Xe) exhibits neuroprotective effects, yet the specific mechanism by which it regulates microglia remains unclear.
methodsPublic transcriptome datasets of human stroke cortex (GSE56267) and Xe-treated microglia (GSE273575) were analyzed, and key genes were screened using machine learning. An oxygen-glucose deprivation/reoxygenation (OGD/R) model was established with human microglial cells (HMC3). NREP expression, microglial polarization, and inflammatory responses were assessed via Western blot, flow cytometry, and ELISA. HMC3 cells were co-cultured with human cortical neurons using Transwell inserts, and neuronal damage was evaluated by CCK-8 assay, kit-based detection, and flow cytometry. Finally, a middle cerebral artery occlusion (MCAO) model was established in rats to investigate the potential involvement of NREP in the neuroprotective effects of Xe in vivo.
resultsNREP was identified as a key regulatory gene that was downregulated after stroke and upregulated following Xe treatment. In the OGD/R model, Xe upregulated NREP expression in HMC3 cells, inhibited M1 polarization and proinflammatory cytokine release, and this effect could be partially reversed by NREP silencing. Xe-treated HMC3 cells mitigated apoptosis and oxidative stress in co-cultured neurons, which appeared to be, at least in part, dependent on NREP. In MCAO rats, Xe upregulated NREP in the brain and reduced infarct volume and neuroinflammation. Critically, in vivo knockdown of NREP significantly reversed these neuroprotective and anti-inflammatory effects of Xe.
conclusionXe treatment upregulated NREP expression, inhibited M1 polarization of microglia and neuroinflammation, and alleviated cerebral ischemia-reperfusion injury in experimental models. These findings suggest that NREP contributes to xenon-mediated neuroprotection and may serve as a potential therapeutic target, providing preliminary experimental evidence for subsequent translational research of IS.
Indexed as
Identifiers
42461351What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.