Evidence map›Paper›PMID 29689082›Full record

ArticlePloS one2018

Propofol induces nuclear localization of Nrf2 under conditions of oxidative stress in cardiac H9c2 cells.

Takeaki Shinjo, Tatsuhide Tanaka, Hiroaki Okuda, Akira T Kawaguchi, Kentaro Oh-Hashi, Yuki Terada, Ayami Isonishi, Shoko Morita-Takemura, Kouko Tatsumi, Masahiko Kawaguchi and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Chrysin protects cardiac H9c2 cells against HMolecular and cellular biochemistry · 2023
    Article
  3. Article
  4. Article
  5. Article
  6. NRF2 in Cardiovascular Diseases: a Ray of Hope!Journal of cardiovascular translational research · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. 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

11 authors at 4 institutions in 1 country.

Takeaki ShinjoDepartment of Anesthesiology, Nara Medical University, Kashihara, Nara, Japan.
Tatsuhide TanakaDepartment of Anatomy and Neuroscience, Nara Medical University, Kashihara, Nara, Japan.ORCID 0000-0002-3373-9093
Hiroaki OkudaDepartment of Functional Anatomy, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa, Japan.
Akira T KawaguchiDepartment of Cell Transplantation and Regenerative Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Kentaro Oh-HashiDepartment of Chemistry and Biomolecular Science, Faculty of Engineering, Gifu University, Gifu, Japan.
Yuki TeradaDepartment of Anesthesiology, Nara Medical University, Kashihara, Nara, Japan.
Ayami IsonishiDepartment of Anatomy and Neuroscience, Nara Medical University, Kashihara, Nara, Japan.
Shoko Morita-TakemuraDepartment of Anatomy and Neuroscience, Nara Medical University, Kashihara, Nara, Japan.
Kouko TatsumiDepartment of Anatomy and Neuroscience, Nara Medical University, Kashihara, Nara, Japan.
Masahiko KawaguchiDepartment of Anesthesiology, Nara Medical University, Kashihara, Nara, Japan.
Akio WanakaDepartment of Anatomy and Neuroscience, Nara Medical University, Kashihara, Nara, Japan.
Nara Medical University · JPGifu University · JPKanazawa University · JPTokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress contributes to myocardial ischemia-reperfusion injury, which causes cardiomyocyte death and precipitate life-threatening heart failure. Propofol has been proposed to protect cells or tissues against oxidative stress. However, the mechanisms underlying its beneficial effects are not fully elucidated. In the present study, we employed an in vitro oxidative injury model, in which rat cardiac H9c2 cells were treated with H2O2, and investigated roles of propofol against oxidative stress. Propofol treatment reduced H2O2-induced apoptotic cell death. While H2O2 induced expression of the antioxidant enzyme HO-1, propofol further increased HO-1 mRNA and protein levels. Propofol also promoted nuclear localization of Nrf2 in the presence of H2O2. Knockdown of Nrf2 using siRNA suppressed propofol-inducible Nrf2 and expression of Nrf2-downstream antioxidant enzyme. Knockdown of Nrf2 suppressed the propofol-induced cytoprotection. In addition, Nrf2 overexpression induced nuclear localization of Nrf2 and HO-1 expression. These results suggest that propofol exerts antioxidative effects by inducing nuclear localization of Nrf2 and expression of its downstream enzyme in cardiac cells. Finally, we examined the effect of propofol on cardiomyocytes using myocardial ischemia-reperfusion injury models. The expression level of Nrf2 protein was increased at 15 min after reperfusion in the ischemia-reperfusion and propofol group compared with ischemia-reperfusion group in penumbra region. These results suggest that propofol protects cells or tissues from oxidative stress via Nrf2/HO-1 cascade.

Indexed as

AnimalsApoptosisCell LineCell NucleusGene Expression RegulationGene Knockdown TechniquesHeme Oxygenase (Decyclizing)Hydrogen PeroxideModels, BiologicalMyocardial Reperfusion InjuryMyocytes, CardiacNF-E2-Related Factor 2Oxidative StressPropofolProtein TransportRatsHeme Oxygenase (Decyclizing)Hmox1 protein, ratHydrogen PeroxideNfe2l2 protein, ratNF-E2-Related Factor 2Propofol

Identifiers

PMID29689082
PMCPMC5915683
OpenAlexW2801243074

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.