Evidence map›Paper›PMID 27081917›Full record

ArticleMolecular medicine reports2016

NQDI-1, an inhibitor of ASK1 attenuates acute perinatal hypoxic-ischemic cerebral injury by modulating cell death.

Hu Hao, Sitao Li, Hui Tang, Bingqing Liu, Yao Cai, Congcong Shi, Xin Xiao

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  5. Review
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  8. Article
  9. The MCBritish journal of pharmacology · 2019
    Article
  10. Review
  11. Review
  12. Article
  13. Cell Death in the Developing Brain after Hypoxia-Ischemia.Frontiers in cellular neuroscience · 2017
    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

7 authors at 3 institutions in 1 country.

Hu HaoDepartment of Pediatrics, The Sixth Affiliated Hospital of Sun Yat‑Sen University, Guangzhou, Guangdong 510655, P.R. China.
Sitao LiDepartment of Pediatrics, The Sixth Affiliated Hospital of Sun Yat‑Sen University, Guangzhou, Guangdong 510655, P.R. China.
Hui TangCentral Laboratory, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630 P.R. China.
Bingqing LiuDepartment of Pediatrics, The Sixth Affiliated Hospital of Sun Yat‑Sen University, Guangzhou, Guangdong 510655, P.R. China.
Yao CaiDepartment of Pediatrics, The Sixth Affiliated Hospital of Sun Yat‑Sen University, Guangzhou, Guangdong 510655, P.R. China.
Congcong ShiDepartment of Pediatrics, The Sixth Affiliated Hospital of Sun Yat‑Sen University, Guangzhou, Guangdong 510655, P.R. China.
Xin XiaoDepartment of Pediatrics, The Sixth Affiliated Hospital of Sun Yat‑Sen University, Guangzhou, Guangdong 510655, P.R. China.
Sixth Affiliated Hospital of Sun Yat-sen University · CNSun Yat-sen University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis signal-regulating kinase 1 (ASK1) is a ubiquitously expressed protein kinase, which regulates cell fate in numerous injury conditions. Therefore, ASK1 may be a promising novel therapeutic target for injury. However, the expression and distribution of ASK1 in the perinatal brain following hypoxia-ischemia (HI) remains to be elucidated. In the present study, western blotting and immunofluorescence were used to determine the expression and distribution of ASK1 and any associated downstream targets in the perinatal rat brain following HI. NQDI‑1, a specific inhibitor of ASK1 was intracerebroventricularly injected following neonatal rats brain insult for neuroprotection. The results revealed an increased expression of ASK1 and this expression was localized to the neurons and astrocytes, compared with the sham controls. Additionally, it was demonstrated that the ASK1/ c‑Jun N‑terminal kinases (JNK) pathway was involved in the brain damage following HI in neonatal rats. Notably, NQDI‑1 significantly inhibited the in vivo expression levels of ASK1, phosphorylated (p‑)JNK, p‑c‑Jun, p53 and caspase 3. Reduced acute hypoxic‑ischemic cerebral injury and cell apoptosis was observed following the injection of NQDI‑1. Collectively, NQDI-1 attenuated acute perinatal hypoxic‑ischemic cerebral injury by inhibiting the expression of ASK1 and cell apoptosis. This may be a promising novel neuroprotective inhibitor for perinatal cerebra injury.

Indexed as

AnimalsApoptosisAporphinesBrainCaspase 3Cell DeathDisease Models, AnimalFemaleGene ExpressionHypoxia-Ischemia, BrainJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase Kinase 5Protein Kinase InhibitorsProto-Oncogene Proteins c-junQuinolinesRats2,7-dioxo-2,7-dihydro-3H-naphtho(1,2,3-de)quinoline-1-carboxylateAporphinesCaspase 3JNK Mitogen-Activated Protein KinasesMAP Kinase Kinase Kinase 5Protein Kinase InhibitorsProto-Oncogene Proteins c-junQuinolinesTumor Suppressor Protein p53

Identifiers

PMID27081917
PMCPMC4878550
OpenAlexW2337045784

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.