Evidence map›Paper›PMID 30669368›Full record

ArticleInternational journal of molecular sciences2019

HADC8 Inhibitor WK2-16 Therapeutically Targets Lipopolysaccharide-Induced Mouse Model of Neuroinflammation and Microglial Activation.

Fan-Li Lin, Jing-Lun Yen, Yu-Cheng Kuo, Jaw-Jou Kang, Yu-Wen Cheng, Wei-Jan Huang, George Hsiao

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Investigation of Anti-Inflammatory Potential ofMolecules (Basel, Switzerland) · 2019
    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

7 authors at 2 institutions in 1 country.

Fan-Li LinSchool of Pharmaceutical Sciences, National Yang-Ming University, Taipei 112-21, Taiwan. fllin@tmu.edu.tw.
Jing-Lun YenGraduate Institute of Medical Sciences and Department of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110-31, Taiwan. m120102039@tmu.edu.tw.
Yu-Cheng KuoGraduate Institute of Medical Sciences and Department of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110-31, Taiwan. yucheng.kuo@msa.hinet.net.
Jaw-Jou KangSchool of Pharmaceutical Sciences, National Yang-Ming University, Taipei 112-21, Taiwan. jjkang@ym.edu.tw.
Yu-Wen ChengSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 110-31, Taiwan. ywcheng@tmu.edu.tw.ORCID 0000-0003-3714-0464
Wei-Jan HuangGraduate Institute of Pharmacognosy, College of Pharmacy, Taipei Medical University, Taipei 110-31, Taiwan. wjhuang@tmu.edu.tw.
George HsiaoGraduate Institute of Medical Sciences and Department of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110-31, Taiwan. geohsiao@tmu.edu.tw.
Taipei Medical University · TWNational Yang Ming Chiao Tung University · TW

Funding

Ministry of Science and Technology, Taiwan 105-2320-B-038-041
6 · The paper itself

Abstract

Glial activation and neuroinflammatory processes play important roles in the pathogenesis of brain abscess and neurodegenerative diseases. Activated glial cells can secrete various proinflammatory cytokines and neurotoxic mediators, which contribute to the exacerbation of neuronal cell death. The inhibition of glial activation has been shown to alleviate neurodegenerative conditions. The present study was to investigate the specific HDAC8 inhibitor WK2-16, especially its effects on the neuroinflammatory responses through glial inactivation. WK2-16 significantly reduced the gelatinolytic activity of MMP-9, and expression of COX-2/iNOS proteins in striatal lipopolysaccharide (LPS)-induced neuroinflammation in C57BL/6 mice. The treatment of WK2-16 markedly improved neurobehavioral deficits. Immunofluorescent staining revealed that WK2-16 reduced LPS-stimulated astrogliosis and microglial activation in situ. Consistently, cellular studies revealed that WK2-16 significantly suppressed LPS-induced mouse microglia BV-2 cell proliferation. WK2-16 was proven to concentration-dependently induce the levels of acetylated SMC3 in microglial BV-2 cells. It also reduced the expression of COX-2/iNOS proteins and TNF-α production in LPS-activated microglial BV-2 cells. The signaling studies demonstrated that WK2-16 markedly inhibited LPS-activated STAT-1/-3 and Akt activation, but not NF-κB or MAPK signaling. In summary, the HADC8 inhibitor WK2-16 exhibited neuroprotective effects through its anti-neuroinflammation and glial inactivation properties, especially in microglia

Indexed as

AnimalsBiomarkersBrainCell LineCytokinesDisease Models, AnimalHistone Deacetylase InhibitorsHistone DeacetylasesInflammationInflammation MediatorsLipopolysaccharidesMaleMiceMicrogliaNervous System DiseasesNeuroprotective AgentsBiomarkersCytokinesHDAC8 protein, mouseHistone Deacetylase InhibitorsHistone DeacetylasesInflammation MediatorsLipopolysaccharidesNeuroprotective AgentsSTAT1 Transcription FactorSTAT3 Transcription FactorAktHDAC8 inhibitormicroglianeuroinflammationSTATWK2-16

Identifiers

PMID30669368
PMCPMC6359084
OpenAlexW2910795022

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.