Evidence map›Paper›PMID 33923922›Full record

ArticleInternational journal of molecular sciences2021

Mangiferin Inhibits Apoptosis in Doxorubicin-Induced Vascular Endothelial Cells via the Nrf2 Signaling Pathway.

Mohammad Bani Ismail, Peramaiyan Rajendran, Hamad Mohammed AbuZahra, Vishnu Priya Veeraraghavan

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Mangiferin Ameliorates CClJournal of inflammation research · 2024
    Article
  11. Article
  12. Review
  13. Review
  14. Optimizing combination therapy in a murine model of HER2+ breast cancer.Computer methods in applied mechanics and engineering · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Article
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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

4 authors at 2 institutions in 2 countries.

Mohammad Bani IsmailDepartment of Biological Sciences, College of Science, King Faisal University, Al Ahsa 31982, Saudi Arabia.
Peramaiyan RajendranDepartment of Biological Sciences, College of Science, King Faisal University, Al Ahsa 31982, Saudi Arabia.ORCID 0000-0001-6354-4388
Hamad Mohammed AbuZahraDepartment of Biological Sciences, College of Science, King Faisal University, Al Ahsa 31982, Saudi Arabia.ORCID 0000-0003-0972-5676
Vishnu Priya VeeraraghavanDepartment of Biochemistry, Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai 600 077, India.
King Faisal University · SASaveetha University · IN

Funding

Deanship of Scientific Research, King Faisal University 216026
6 · The paper itself

Abstract

Doxorubicin increases endothelial permeability, hence increasing cardiomyocytes' exposure to doxorubicin (DOX) and exposing myocytes to more immediate damage. Reactive oxygen species are major effector molecules of doxorubicin's activity. Mangiferin (MGN) is a xanthone derivative that consists of C-glucosylxanthone with additional antioxidant properties. This particular study assessed the effects of MGN on DOX-induced cytotoxicity in human umbilical vein endothelial cells' (HUVECs') signaling networks. Mechanistically, MGN dramatically elevated Nrf2 expression at both the messenger RNA and protein levels through the upregulation of the PI3K/AKT pathway, leading to an increase in Nrf2-downstream genes. Cell apoptosis was assessed with a caspase-3 activity assay, transferase-mediated dUTP-fluorescein nick end labeling (TUNEL) staining was performed to assess DNA fragmentation, and protein expression was determined by Western blot analysis. DOX markedly increased the generation of reactive oxygen species, PARP, caspase-3, and TUNEL-positive cell numbers, but reduced the expression of Bcl-2 and antioxidants' intracellular concentrations. These were effectively antagonized with MGN (20 μM), which led to HUVECs being protected against DOX-induced apoptosis, partly through the PI3K/AKT-mediated NRF2/HO-1 signaling pathway, which could theoretically protect the vessels from severe DOX toxicity.

Indexed as

AntioxidantsApoptosisBlotting, WesternCell SurvivalDNA FragmentationDoxorubicinFluorescent Antibody TechniqueHumansHuman Umbilical Vein Endothelial CellsIn Situ Nick-End LabelingNF-E2-Related Factor 2Oxidative StressReactive Oxygen SpeciesSignal TransductionXanthonesAntioxidantsDoxorubicinmangiferinNF-E2-Related Factor 2Reactive Oxygen SpeciesXanthonesapoptosisdoxorubicinmangiferinNrf2oxidative stressreactive oxygen species

Identifiers

PMID33923922
PMCPMC8073066
OpenAlexW3154122321

What OpenQuestion holds

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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.