Evidence map›Paper›PMID 38346718›Full record

ArticleBrain and behavior2024

Calcitriol restrains microglial M1 polarization and alleviates dopaminergic degeneration in hemiparkinsonian mice by boosting regulatory T-cell expansion.

Yangzhi Xie, Liang Chen, Jiacheng Chen, Yongjun Chen

Open access · goldAbstract read
In one paragraph

Article in Brain and behavior, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 9 citations in OpenAlex.

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  7. Effect of Sphingomyelin and Vitamin D3 Intake on the Rabbit Brain.International journal of molecular sciences · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Yangzhi XieDepartment of Neurology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang, China.ORCID 0000-0003-2248-9719
Liang ChenDepartment of Neurology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang, China.
Jiacheng ChenDepartment of Intensive Care Unit, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang, China.
Yongjun ChenDepartment of Neurology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang, China.
University of South China · CN

Funding

Key Project of Hunan Provincial Health and Health Commission in 2020 20201910
6 · The paper itself

Abstract

objectiveVitamin D deficiency is a risk factor for Parkinson's disease (PD) and vitamin D supplementation robustly alleviates neurodegeneration in PD models. However, the mechanisms underlying this effect require further clarification. Current evidence suggests that harnessing regulatory T cells (Treg) may mitigate neuronal degeneration. In this study, we investigated the therapeutic effects of vitamin D receptor activation by calcitriol on PD, specifically focusing on its role in Treg.

methodsHemiparkinsonian mice model was established through the injection of 6-OHDA into the striatum. Mice were pretreated with calcitriol before 6-OHDA injection. The motor performance, dopaminergic neuronal survival, contents of dopamine, and dopamine metabolites were evaluated. The pro-inflammatory cytokines levels, T-cell infiltration, mRNA expression of indicated microglial M1/M2 phenotypic markers, and microglial marker in the midbrain were detected. Populations of Treg in the splenic tissues were assessed using a flow cytometry assay. PC61 monoclonal antibody was applied to deplete Treg in vivo.

resultsWe show that calcitriol supplementation notably improved motor performance and reduced dopaminergic degeneration in the 6-OHDA-induced PD model. Mechanistically, calcitriol promoted anti-inflammatory/neuroprotective Treg and inhibited pro-inflammatory/neurodestructive effector T-cell generation in this model. This process significantly inhibited T-cell infiltration in the midbrain, restrained microglial activation, microglial M1 polarization, and decreased pro-inflammatory cytokines release. This more favorable inflammatory microenvironment rescued dopaminergic degeneration. To further verify that the anti-inflammatory effects of calcitriol are associated with Treg expansion, we applied an antibody-mediated Treg depletion assay. As predicted, the anti-inflammatory effects of calcitriol in the PD model were diminished following Treg depletion.

conclusionThese findings suggest that calcitriol's anti-inflammatory and neuroprotective effects in PD are associated with its potential to boost Treg expansion.

Indexed as

MicrogliaParkinson DiseaseAnimalsAnti-Inflammatory AgentsCalcitriolCytokinesDisease Models, AnimalDopamineDopaminergic NeuronsMiceMice, Inbred C57BLOxidopamineT-Lymphocytes, RegulatoryAnti-Inflammatory AgentsCalcitriolCytokinesDopamineOxidopamineM1/M2 polarizationneuroinflammationParkinson's diseaseregulatory T cellvitamin D receptor

Identifiers

PMID38346718
PMCPMC10861354
OpenAlexW4392316602

What OpenQuestion holds

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Registered trials

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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.