ArticleNeurochemical research2026
Ginsenoside Rb1 Maintains Tunneling Nanotubes between Astrocytes and Neurons To Protect Mice from Cerebral ischemia/reperfusion Injury.
Article in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed.
- Endothelial energy failure as a therapeutic target in elderly strokes.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Ginsenoside Rb1 (GRb1), the major bioactive component of ginseng, exhibits multiple therapeutic effects. However, its neuroprotective role in cerebral ischemia/reperfusion (I/R) injury remains unclear. The neuroprotective effects of GRb1 were investigated using a mouse middle cerebral artery occlusion (MCAO) model and in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) models. GRb1 was administered intraperitoneally to MCAO mice, and the effects on neurological function, brain edema, blood-brain barrier (BBB) integrity, and extracellular matrix (ECM) remodeling were evaluated. In the OGD/R model, tunneling nanotubes (TnTs) formation, oxidative stress, and mitochondrial integrity were evaluated in a co-culture of astrocytes and neurons. GRb1 markedly enhanced neurological function, alleviated brain edema, and maintained BBB integrity in MCAO mice. It also inhibited the expression of matrix metalloproteinases and Granzyme B while increasing Serpina3n, indicating protection of ECM integrity. In OGD/R-treated neurons, GRb1 reduced oxidative stress, restored superoxide dismutase activity, and preserved ATP and mitochondrial DNA. Importantly, GRb1 significantly enhanced TnTs formation, and inhibition of TnTs with cytochalasin B markedly reversed these protective effects, supporting a TnT-dependent mechanism. GRb1 effectively protected against I/R-induced neuronal injury through TnTs-dependent mechanisms, modulating oxidative stress, ECM remodeling, and mitochondrial integrity.
Indexed as
Identifiers
41528388What 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.