Evidence map›Paper›PMID 29675728›Full record

ArticleNeurochemical research2018

Histone Deacetylase 2 Inhibitor CAY10683 Alleviates Lipopolysaccharide Induced Neuroinflammation Through Attenuating TLR4/NF-κB Signaling Pathway.

Fang-Zhou Jiao, Yao Wang, Hai-Yue Zhang, Wen-Bin Zhang, Lu-Wen Wang, Zuo-Jiong Gong

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Neuroinflammation in Alzheimer disease.Nature reviews. Immunology · 2025
    Review
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  11. Epigenetics of Cutaneous Sarcoma.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Review
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  15. Review
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  17. Review
  18. Article
  19. Article
  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

6 authors at 2 institutions in 1 country.

Fang-Zhou JiaoDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Yao WangDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Hai-Yue ZhangDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Wen-Bin ZhangDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Lu-Wen WangDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Zuo-Jiong GongDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, 430060, China. zjgong@163.com.
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

National Natural Science Foundation of China No. 81371789
6 · The paper itself

Abstract

Neuroinflammation involves in the progression of many central nervous system diseases. Several studies have shown that histone deacetylase (HDAC) inhibitors modulated inflammatory responses in lipopolysaccharide (LPS) stimulated microglia. While, the mechanism is still unclear. The aim of present study was to investigate the effect of HDAC2 inhibitor CAY10683 on inflammatory responses and TLR4/NF-κB signaling pathways in LPS activated BV2 microglial cells and LPS induced mice neuroinflammation. The effect of CAY10683 on cell viability of BV2 microglial cells was detected by CCK-8 assay. The expressions of inflammatory cytokines were analyzed by western blotting and RT-PCR respectively. The TLR4 protein expression was measured by western blotting, immunofluorescence, immunohistochemistry respectively. The protein expressions of MYD88, phospho-NF-κB p65, NF-κB-p65, acetyl-H3 (AH3), H3, and HDAC2 were analyzed by western blotting. We found that CAY10683 could inhibit expression levels of inflammatory cytokine TNF-α and IL-1β in LPS activated BV2 microglial cells and LPS induced mice neuroinflammation. It could induce TLR4, MYD88, phospho-NF-κB p65, and HDAC2 expressions. Moreover, CAY10683 increased the acetylation of histones H3 in LPS activated BV2 microglial cells and LPS induced mice neuroinflammation. Taken together, our findings suggested that HDAC2 inhibitor CAY10683 could suppress neuroinflammatory responses and TLR4/NF-κB signaling pathways by acetylation after LPS stimulation.

Indexed as

AnimalsCell LineHistone Deacetylase 2Histone Deacetylase InhibitorsInflammation MediatorsLipopolysaccharidesMiceMicrogliaNF-kappa BRandom AllocationSignal TransductionToll-Like Receptor 4Histone Deacetylase 2Histone Deacetylase InhibitorsInflammation MediatorsLipopolysaccharidesNF-kappa BTlr4 protein, mouseToll-Like Receptor 4Histone deacetylaseMicrogliaNeuroinflammationNF-κB-p65TLR4

Identifiers

PMID29675728
OpenAlexW2802588821

What OpenQuestion holds

Textmetadata
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.