ArticleCurrent medical science2025
Vitamin D Activates Nrf2 to Prevent Nerve Injury and Reduce Brain Damage in Acute Cerebral Infarction.
Article in Current medical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Vitamin D Receptor Polymorphisms and Their Association with Nrf2-Dependent Gene Expression in Oxidative Stress Resilience in Cognitively Healthy Aging.Antioxidants (Basel, Switzerland) · 2026Article
- Vitamin D Promotes Neuronal Survival via Nrf2 Upregulation in D-Galactose-Induced Mice: An In-Vivo and In-Silico Study.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Vitamin D Signaling in Neurodegenerative Disorders: Mechanisms, Therapeutic Potential, and Clinical Implications.Nutrients · 2026Review
- The Role of Vitamin D in Neuropathic Pain: Biological Mechanisms and Clinical Relevance.International journal of molecular sciences · 2026Review
- A vitamin-biomarker risk score for 90-day functional outcome after acute ischemic stroke: development and internal validation in a retrospective cohort.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
objectiveThis study aimed to investigate the neuroprotective effects of cholecalciferol cholesterol emulsion (CCE), a vitamin D (VD) precursor, in a murine model of acute cerebral infarction (ACI) and to elucidate the role of the Nrf2 signaling pathway in mediating these effects.
methodsForty C57BL/6J mice (male and female) were divided into five groups (n = 10 per group): control, control + CCE, ACI, ACI + CCE, and ACI + CCE + ML385 (an Nrf2 inhibitor). ACI was induced by middle cerebral artery occlusion (MCAO). CCE was administered for three weeks prior to ACI induction, and ML385 was administered intravenously to inhibit Nrf2. Neurological function, brain edema, and infarct size, as well as inflammatory and apoptotic marker levels, were assessed post-ACI. Statistical analyses were conducted via one-way ANOVA and Student's t test, with P < 0.05 considered significant.
resultsCompared to ACI group, CCE significantly reduced neurological deficits, brain edema, and infarct size (P < 0.01). The ACI + CCE group presented improved short-term memory retention, as evidenced by shorter avoidance latency in shuttle avoidance tests (P < 0.01). CCE administration attenuated the expression of inflammatory markers (IL-6, MIF, Lp-PLA2) while increasing IL-10 levels (P < 0.001). Furthermore, CCE increased Nrf2 and HO-1 expression and reduced apoptosis by decreasing the Bax/Bcl-2 ratio in brain tissue (P < 0.001). ML385 abolished these neuroprotective effects, confirming the role of the Nrf2 pathway in mediating the benefits of VD.
conclusionVD, via VD receptor-mediated activation of the Nrf2/HO-1 pathway, reduces inflammation, apoptosis, and neurological damage following ACI. These findings support the therapeutic potential of VD in the treatment of ischemic stroke and highlight the importance of Nrf2 in mediating these effects.
Indexed as
Identifiers
40332737What 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.