Evidence map›Paper›PMID 26604696›Full record

ArticleDrug design, development and therapy2015

Mechanisms underlying the perifocal neuroprotective effect of the Nrf2-ARE signaling pathway after intracranial hemorrhage.

Xiao-Ping Yin, Zhi-Ying Chen, Jun Zhou, Dan Wu, Bing Bao

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Potential therapeutic effects of Nrf2 activators on intracranial hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Sulforaphane Protects against Brain Diseases: Roles of Cytoprotective Enzymes.Austin journal of cerebrovascular disease & stroke · 2017
    Article
  19. Review
  20. Review
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

5 authors at 2 institutions in 1 country.

Xiao-Ping YinDepartment of Neurology, The Second Affiliated Hospital of Nanchang University, Nanchang, People's Republic of China ; Department of Neurology, Affiliated Hospital of Jiujiang University, Jiujiang, People's Republic of China.
Zhi-Ying ChenDepartment of Neurology, Affiliated Hospital of Jiujiang University, Jiujiang, People's Republic of China.
Jun ZhouDepartment of Neurology, The Second Affiliated Hospital of Nanchang University, Nanchang, People's Republic of China.
Dan WuDepartment of Neurology, The Second Affiliated Hospital of Nanchang University, Nanchang, People's Republic of China ; Department of Neurology, The Sixth Hospital of Wuhan, Wuhan, People's Republic of China.
Bing BaoDepartment of Neurology, Affiliated Hospital of Jiujiang University, Jiujiang, People's Republic of China.
Second Affiliated Hospital of Nanchang University · CNJiujiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt has been found that nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2-ARE) signaling pathway plays a role in antioxidative response, anti-inflammatory response, and neuron-protection in intracerebral hemorrhage (ICH). The aim of this study is to explore mechanisms underlying the perifocal neuroprotective effect of the Nrf2-ARE signaling pathway after ICH.

methodsThere were a total of 90 rats with basal ganglia hemorrhage, which were randomly divided into the following four groups: ICH (Sprague-Dawley rats with autologous femoral arterial blood injection into the basal ganglia), sulforaphane (SFN) (SFN was intraperitoneally administered into rats), retinoic acid (RA) (RA was intraperitoneally administered into rats), and dimethyl sulfoxide (the rats were treated with dimethyl sulfoxide). We observed the neurological score of the rats in the different groups, and collected brain tissues for immunofluorescence, Western blot, and reverse transcription polymerase chain reaction to detect expression of Nrf2, heme oxygenase (HO-1), nuclear factor-κB (NF-κB), and tumor necrosis factor-α (TNF-α).

resultsThe results indicated that neurological dysfunction of rats was significantly improved in the SFN group, and the expressions of Nrf2 and HO-1 in tissues surrounding the hemorrhage were increased. Also, the level of NF-κB and TNF-α were reduced compared to the ICH group. The RA group exhibited more severe neurological dysfunction and lower levels of Nrf2 and HO-1 than the SFN and ICH groups. Compared to the ICH group, the NF-κB and TNF-α expression in the RA groups was increased. In conclusion, RA inhibits Nrf2 dissociation and translocation into nucleus, thereby suppressing the anti-inflammatory effect of Nrf2-ARE signaling pathway. The activation of Nrf2-ARE signaling pathway by SFN can elevate expression of antioxidant enzyme HO-1, reduce perifocal inflammatory response after ICH, and thus may play a neuroprotective role.

conclusionThe results suggest that Nrf2-ARE signaling pathway may serve as a new target for treatment of perifocal inflammatory injury caused by ICH.

Indexed as

AnimalsAntioxidant Response ElementsBlotting, WesternCerebral HemorrhageDimethyl SulfoxideDisease Models, AnimalHeme Oxygenase-1IsothiocyanatesMaleNeuroprotectionNF-E2-Related Factor 2NF-kappa BRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionSignal TransductionDimethyl SulfoxideHeme Oxygenase-1IsothiocyanatesNF-E2-Related Factor 2NF-kappa BsulforaphaneSulfoxidesTretinoinTumor Necrosis Factor-alphaantioxidant response elementscerebral hemorrhageinjuriesNF-E2-related factor 2

Identifiers

PMID26604696
PMCPMC4655949
OpenAlexW2204630116

What OpenQuestion holds

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LicenceCC BY-NC
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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.