Evidence map›Paper›PMID 24621589›Full record

ArticlePloS one2014

Anti-neuroinflammatory effects of the calcium channel blocker nicardipine on microglial cells: implications for neuroprotection.

Bor-Ren Huang, Pei-Chun Chang, Wei-Lan Yeh, Chih-Hao Lee, Cheng-Fang Tsai, Chingju Lin, Hsiao-Yun Lin, Yu-Shu Liu, Caren Yu-Ju Wu, Pei-Ying Ko and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 9% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 citations in OpenAlex.

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  20. L-Type CaInternational journal of molecular sciences · 2022
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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

13 authors at 7 institutions in 2 countries.

Bor-Ren HuangGraduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan; Neurosurgery Department, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, Taiwan; School of Medicine, Tzu Chi University, Hualien, Taiwan.
Pei-Chun ChangDepartment of Bioinformatics, Asia University, Taichung, Taiwan.
Wei-Lan YehDepartment of Cell and Tissue Engineering, Changhua Christian Hospital, Changhua, Taiwan.
Chih-Hao LeeDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, United States of America.
Cheng-Fang TsaiDepartment of Biotechnology, Asia University, Taichung, Taiwan.
Chingju LinDepartment of Physiology, School of Medicine, China Medical University, Taichung, Taiwan.
Hsiao-Yun LinDepartment of Life Sciences, National Chung Hsing University, Taichung, Taiwan.
Yu-Shu LiuGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Caren Yu-Ju WuGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Pei-Ying KoDepartment of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan.
Shiang-Suo HuangDepartment of Pharmacology and Institute of Medicine, College of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Horng-Chaung HsuGraduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan; Department of Orthopedic Surgery, China Medical University Hospital, Taichung, Taiwan.
Dah-Yuu LuGraduate Institute of Neural and Cognitive Sciences, China Medical University, Taichung, Taiwan.
China Medical University · TWAsia University · TWBoston University · USChanghua Christian Hospital · TWChung Shan Medical University · TWNational Chung Hsing University · TWTaipei Tzu Chi Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectiveNicardipine is a calcium channel blocker that has been widely used to control blood pressure in severe hypertension following events such as ischemic stroke, traumatic brain injury, and intracerebral hemorrhage. However, accumulating evidence suggests that inflammatory processes in the central nervous system that are mediated by microglial activation play important roles in neurodegeneration, and the effect of nicardipine on microglial activation remains unresolved. METHODOLOGY/PRINCIPAL

findingsIn the present study, using murine BV-2 microglia, we demonstrated that nicardipine significantly inhibits microglia-related neuroinflammatory responses. Treatment with nicardipine inhibited microglial cell migration. Nicardipine also significantly inhibited LPS plus IFN-γ-induced release of nitric oxide (NO), and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Furthermore, nicardipine also inhibited microglial activation by peptidoglycan, the major component of the Gram-positive bacterium cell wall. Notably, nicardipine also showed significant anti-neuroinflammatory effects on microglial activation in mice in vivo. CONCLUSION/SIGNIFICANCE: The present study is the first to report a novel inhibitory role of nicardipine on neuroinflammation and provides a new candidate agent for the development of therapies for inflammation-related neurodegenerative diseases.

Indexed as

AnimalsBlood PressureCalcium Channel BlockersCell LineCytokinesGene Expression RegulationInflammationMiceMicrogliaNeuroprotective AgentsNicardipineSignal TransductionCalcium Channel BlockersCytokinesNeuroprotective AgentsNicardipine

Identifiers

PMID24621589
PMCPMC3951295
OpenAlexW2135957157

What OpenQuestion holds

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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.