Evidence map›Paper›PMID 26259787›Full record

ArticleJournal of neuroinflammation2015

1,25-Dihydroxyvitamin D3 attenuates endotoxin-induced production of inflammatory mediators by inhibiting MAPK activation in primary cortical neuron-glia cultures.

Ya-Ni Huang, Yi-Jung Ho, Chien-Cheng Lai, Chien-Tsai Chiu, Jia-Yi Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 3 pooled it
6.4field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 3 syntheses or guidelines pooled it, 71 citations in OpenAlex.

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  9. Effects of Vitamin D Supplementation on Children with Autism Spectrum Disorder: A Systematic Review and Meta-analysis.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2023
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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

5 authors at 5 institutions in 1 country.

Ya-Ni HuangDepartment of Nursing, Hsin Sheng Junior College of Medical Care and Management, Taoyuan City, Taiwan. yani0106@gmail.com.
Yi-Jung HoInstitute of Preventive Medicine, National Defense Medical Center, Taipei, Taiwan. ejung330@gmail.com.
Chien-Cheng LaiDivision of Orthopedics, Department of Surgery, Far Eastern Memorial Hospital, New Taipei City, Taiwan. popula180@gmail.com.
Chien-Tsai ChiuDepartment of Neurosurgery, En Chu Kong Hospital, New Taipei City, Taiwan. chientsaichiu@hotmail.com.
Jia-Yi WangGraduate Institute of Medical Sciences and Department of Physiology, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei, 110, Taiwan. jywang2010@tmu.edu.tw.
En Chu Kong Hospital · TWFar Eastern Memorial Hospital · TWHsin Sheng College of Medical Care and Management · TWNational Defense Medical Center · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroinflammation occurs in insulted regions of the brain and may be due to reactive oxygen species (ROS), nitric oxide (NO), cytokines, and chemokines produced by activated glia. Excessive production of neurotoxic molecules causes further neuronal damage. Low levels of vitamin D3 are a risk factor for various brain diseases.

methodsUsing the bacterial endotoxin, lipopolysaccharide (LPS), to induce neuroinflammation in primary cortical neuron-glia cultures, we investigated how 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) affected neuroinflammation.

resultsLPS (100 ng/ml) induced the accumulation of nitrite and the production of ROS, interleukin (IL)-6, and macrophage inflammatory protein (MIP)-2 in time-dependent manners. Inhibition of p38 and extracellular signal-regulated kinase (ERK) but not c-Jun N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) by 20 μM of SB203580, PD98059, and SP600125, significantly reduced LPS-induced ROS production, NO accumulation, and inducible NO synthase (iNOS) expression, respectively. LPS-induced IL-6 and MIP-2 were significantly attenuated by inhibition of p38, ERK, and JNK MAPK. Cotreatment with 1,25(OH)2D3 attenuated LPS-induced ROS production, NO accumulation, and iNOS expression in concentration-dependent manners. 1,25(OH)2D3 also reduced LPS-induced production of IL-6 and MIP-2. Similarly, iNOS, IL-6, and MIP-2 mRNA expression in cells treated with LPS significantly increased, whereas this effect was attenuated by 1,25(OH)2D3. Moreover, LPS-induced phosphorylation of p38, ERK, and JNK MAPK was significantly inhibited by 1,25(OH)2D3.

conclusionsOur findings indicate that 1,25(OH)2D3 reduced the LPS-stimulated production of inflammatory molecules in neuron-glia cultures by inhibiting MAPK pathways and the production of downstream inflammatory molecules. We suggest that 1,25(OH)2D3 can be used to alleviate neuroinflammation in various brain injuries.

Indexed as

AnimalsAntioxidantsCalcitriolCerebral CortexChemokine CXCL2Enzyme ActivationInflammation MediatorsInterleukin-6LipopolysaccharidesMAP Kinase Signaling SystemMitogen-Activated Protein KinasesNeurogliaNeuronsNitric Oxide Synthase Type IIPrimary Cell CultureRatsAntioxidantsCalcitriolChemokine CXCL2Inflammation MediatorsInterleukin-6LipopolysaccharidesMitogen-Activated Protein KinasesNitric Oxide Synthase Type IIReactive Oxygen SpeciesVitamins

Identifiers

PMID26259787
PMCPMC4532256
OpenAlexW1908848600

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.