ArticleMetabolic brain disease2026
Mild hypothermia inhibits the inflammatory response and microglial M1 polarization in ischemic stroke via the EFNB2/EphB4 pathway.
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
7 authors.
Funding
Abstract
backgroundMild hypothermia (MH) has been reported to ameliorate cerebral damage and neurofunctional deficits in ischemic stroke, but its molecular mechanisms remain unclear. This study focuses on exploring the neuroprotective regulatory mechanisms mediated by MH in ischemic stroke.
methodsA middle cerebral artery occlusion (MCAO) model in vivo was established. MCAO model and LPS-induced microglial cell model were treated with EphB4 kinase inhibitor NVP-BHG712. Brain tissue damage was assessed through 2,3,5-triphenyl tetrazolium chloride (TTC) staining, infarct volume measurement, and brain edema evaluation. Neurological and behavioral functions were evaluated via the rotarod test, grip test, Elevated body swing test (EBST) and neurological deficit scores. Immunofluorescence staining was employed to quantify M1 microglial polarization in brain tissues. The expression of M1 microglial markers and pro-inflammatory cytokines were analyzed by qRT-PCR. Furthermore, qRT-PCR and Western blotting were utilized to quantify key components of the EFNB2/EphB4 signaling axis.
resultsMH significantly attenuated cerebral infarct volume, ameliorated neuromotor deficits, and alleviated cerebral edema in MCAO mice model. Histopathological analyses revealed that MH suppressed neuroinflammation by reducing M1-polarized microglial infiltration and downregulating M1-specific markers (CD16, IBA-1, CD32, CD86). Concurrently, MH inhibited the release of pro-inflammatory cytokines IL-1β and IL-18. In vitro, MH attenuated (LPS)-induced microglial M1 polarization and inflammation. Moreover, hypothermia upregulated EFNB2/EphB4 signaling pathways in both models. Importantly, pharmacological inhibition of EFNB2 abrogated the anti-inflammatory function and neuroprotective effects.
conclusionMH exerts neuroprotective effects by modulating the EFNB2/EphB4 signaling pathway, attenuating post-ischemic neuroinflammation and ameliorating secondary brain injury in ischemic stroke.
Indexed as
Identifiers
42159828What 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.