Evidence map›Paper›PMID 31392841›Full record

ArticleCNS neuroscience & therapeutics2019

Inhibition of activator protein 1 attenuates neuroinflammation and brain injury after experimental intracerebral hemorrhage.

Chang-Juan Wei, Yu-Lin Li, Zi-Long Zhu, Dong-Mei Jia, Mo-Li Fan, Ting Li, Xue-Jiao Wang, Zhi-Guo Li, Hong-Shan Ma

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. AP-1 activates KCNN4-mediated Ca2Cell biology and toxicology · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Antineuroinflammatory Effect ofOxidative medicine and cellular longevity · 2022
    Article
  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

9 authors at 4 institutions in 1 country.

Chang-Juan WeiTianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Yu-Lin LiTianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Zi-Long ZhuDepartment of Neurology, Tianjin Huanhu Hospital, Tianjin, China.
Dong-Mei JiaTianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Mo-Li FanTianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Ting LiTianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Xue-Jiao WangCenter for Neurological Diseases, The Third People's Hospital of Datong, Datong, China.
Zhi-Guo LiTianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.ORCID 0000-0002-6869-2766
Hong-Shan MaCenter for Neurological Diseases, The Third People's Hospital of Datong, Datong, China.
Tianjin Medical University General Hospital · CNShanxi Datong University · CNCapital Medical University · CNTianjin Huanhu Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsIntracerebral hemorrhage (ICH) is a devastating type of stroke without specific treatment. Activator protein 1 (AP-1), as a gene regulator, initiates cytokine expression in response to environmental stimuli. In this study, we investigated the relationship between AP-1 and neuroinflammation-associated brain injury triggered by ICH.

methodsIntracerebral hemorrhage mice were developed by autologous blood or collagenase infusion. We measured the dynamics of AP-1 in mouse brain tissues during neuroinflammation formation after ICH. The effects of the AP-1 inhibitor SR11302 on brain injury and neuroinflammation as well as the underlying mechanisms were investigated in vivo and in vitro.

resultsAP-1 was significantly upregulated in mouse brain tissue as early as 6 hours after ICH, accompanied by elevations in proinflammatory factors, including interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α. Inhibition of AP-1 using SR11302 reduced neurodeficits and brain edema at day 3 after ICH. SR11302 ablated microglial IL-6 and TNF-α production and brain-infiltrating leukocytes in ICH mice. In addition, SR11302 treatment diminished thrombin-induced production of IL-6 and TNF-α in cultured microglia.

conclusionsInhibition of AP-1 curbs neuroinflammation and reduces brain injury following ICH.

Indexed as

AnimalsBrain InjuriesCerebral HemorrhageInflammation MediatorsMaleMiceMice, Inbred C57BLRetinoidsTranscription Factor AP-1Inflammation MediatorsRetinoidsSR 11302Transcription Factor AP-1activator protein 1brain injuryintracerebral hemorrhagemicroglianeuroinflammation

Identifiers

PMID31392841
PMCPMC6776742
OpenAlexW2967815514

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.