Evidence map›Paper›PMID 30479742›Full record

ArticleCell & bioscience2018

(+)-JQ1 attenuated LPS-induced microglial inflammation via MAPK/NFκB signaling.

Huanhuan Wang, Wenhai Huang, Meihao Liang, Yingying Shi, Chixiao Zhang, Qin Li, Meng Liu, Yikai Shou, Hongping Yin, Xiaozheng Zhu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

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  15. MAPK/MAK/MRK overlapping kinase (MOK) controls microglial inflammatory/type-I IFN responses via Brd4 and is involved in ALS.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Review
  17. Review
  18. Review
  19. Dual HDAC/BRD4 Inhibitors Relieves Neuropathic Pain by Attenuating Inflammatory Response in Microglia After Spared Nerve Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
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  20. Article
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 2 institutions in 1 country.

Huanhuan Wang *1School of Medicine, Hangzhou Normal University, Hangzhou, China.
Wenhai Huang *2Institute of Materia Medica, Zhejiang Academy of Medical Sciences, No. 182, Tianmushan Road, Hangzhou, 310013 China.
Meihao Liang2Institute of Materia Medica, Zhejiang Academy of Medical Sciences, No. 182, Tianmushan Road, Hangzhou, 310013 China.
Yingying Shi1School of Medicine, Hangzhou Normal University, Hangzhou, China.
Chixiao Zhang2Institute of Materia Medica, Zhejiang Academy of Medical Sciences, No. 182, Tianmushan Road, Hangzhou, 310013 China.
Qin Li2Institute of Materia Medica, Zhejiang Academy of Medical Sciences, No. 182, Tianmushan Road, Hangzhou, 310013 China.
Meng Liu1School of Medicine, Hangzhou Normal University, Hangzhou, China.
Yikai Shou1School of Medicine, Hangzhou Normal University, Hangzhou, China.
Hongping Yin1School of Medicine, Hangzhou Normal University, Hangzhou, China.
Xiaozheng Zhu1School of Medicine, Hangzhou Normal University, Hangzhou, China.
Xiaoyan Sun3School of Information Science and Engineering, Hangzhou Normal University, Hangzhou, China.
Yu Hu1School of Medicine, Hangzhou Normal University, Hangzhou, China.
Zhengrong Shen2Institute of Materia Medica, Zhejiang Academy of Medical Sciences, No. 182, Tianmushan Road, Hangzhou, 310013 China.ORCID 0000-0002-5383-4397
Hangzhou Normal University · CNZhejiang Academy of Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroglia activation is a crucial event in neurodegenerative disease. The depression of microglial inflammatory response is considered a promising therapeutic strategy. NFκB signaling, including IKK/IκB phosphotylation, p65 nucelus relocalization and NFκB-related genes transcription are prevalent accepted to play important role in microglial activation. (+)-JQ1, a BRD4 inhibitor firstly discovered as an anti-tumor agent, was later confirmed to be an anti-inflammatory compound. However, its anti-inflammatory effect in microglia and central neural system remains unclear.

resultsIn the current work, microglial BV2 cells were applied and treatment with lipopolysaccharide (LPS) to induce inflammation and later administered with (+)-JQ1. In parallel, LPS and (+)-JQ1 was intracerebroventricular injected in IL-1β-luc transgenic mice, followed by fluorescence evaluation and brain tissue collection. Results showed that (+)-JQ1 treatment could significantly reduce LPS induced transcription of inflammatory cytokines both in vitro and in vivo. (+)-JQ1 could inhibit LPS induced MAPK but not PI3K signaling phosphorylation, NFκB relocalization and transcription activity. In animal experiments, (+)-JQ1 postponed LPS induced microglial and astrocytes activation, which was also dependent on MAPK/NFκB signaling.

conclusionsThus, our data demonstrated that (+)-JQ1 could inhibit LPS induced microglia associated neuroinflammation, via the attenuation of MAPK/NFκB signaling.

Indexed as

(+)-JQ1LipopolysaccharideMAPKMicrogliaNFκB

Identifiers

PMID30479742
PMCPMC6245926
OpenAlexW2900858012

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.