ArticleNeurochemical research2026
Electroacupuncture Ameliorates Neuroinflammatory Damage and Cognitive Impairment in Vascular Dementia by Promoting Shh Signaling-Mediated Microglial M2 Polarization.
Article in Neurochemical research, 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
Abstract
Electroacupuncture (EA) has been documented to exert therapeutic benefits in vascular dementia (VD). This study seeks to elucidate the therapeutic efficacy and underlying molecular mechanisms of EA in VD. A VD model was induced in rats, which received EA with or without an Shh pathway inhibitor. An in vitro VD model was generated by exposing BV2 microglial cells to oxygen-glucose deprivation (OGD). A battery of tests was employed: cognitive function (novel object recognition and morris water maze), histopathology (H&E and TUNEL staining), synaptic ultrastructure (transmission electron microscope), microglial activation/polarization (immunofluorescence), inflammatory cytokine secretion (ELISA), protein expression (immunoblotting), and cellular viability (CCK-8). VD model rats exhibited attenuated Shh signaling in brain tissues, which was effectively restored by EA treatment in a duration-dependent manner. EA intervention observably improved cognitive performance, mitigated neuronal damage, enhanced synaptic plasticity, suppressed pro-inflammatory responses, and promoted microglial M2 polarization. These therapeutic effects were abolished by the Shh pathway inhibitor cyclopamine. Furthermore, Shh overexpression in microglia attenuated OGD-induced pro-inflammatory activation and reduced its detrimental impact on neuronal cells. Collectively, these data indicate that the cognitive benefits of EA in VD are critically dependent on Shh-driven reprogramming of microglial responses, which in turn resolves neuroinflammation and mitigates neuronal injury, thereby informing future therapeutic strategies.
Indexed as
Identifiers
42301370What Socratic 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 Socratic graph.