Evidence map›Paper›PMID 27551485›Full record

ArticleCell death discovery2015

Selective cytoprotective effect of histamine on doxorubicin-induced hepatic and cardiac toxicity in animal models.

D J Martinel Lamas, M B Nicoud, H A Sterle, E Carabajal, F Tesan, J C Perazzo, G A Cremaschi, E S Rivera, V A Medina

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Frontiers in pharmacology · 2026
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  5. Foods (Basel, Switzerland) · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Histamine receptors and cancer pharmacology: an update.British journal of pharmacology · 2020
    Review
  13. Article
  14. Article
  15. Review
  16. 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 3 institutions in 1 country.

D J Martinel LamasLaboratory of Radioisotopes, School of Pharmacy and Biochemistry, University of Buenos Aires, Junín 956 PB, Buenos Aires, Argentina; Laboratory of Cellular and Molecular Biology, Institute for Biomedical Research (BIOMED), School of Medical Sciences, Pontifical Catholic University of Argentina (UCA), and the National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina.
M B NicoudLaboratory of Cellular and Molecular Biology, Institute for Biomedical Research (BIOMED), School of Medical Sciences, Pontifical Catholic University of Argentina (UCA), and the National Scientific and Technical Research Council (CONICET) , Buenos Aires, Argentina.
H A SterleNeuroimmunomodulation and Molecular Oncology Division, Institute for Biomedical Research (BIOMED), School of Medical Sciences, Pontifical Catholic University of Argentina (UCA), and the National Scientific and Technical Research Council (CONICET) , Buenos Aires, Argentina.
E CarabajalLaboratory of Radioisotopes, School of Pharmacy and Biochemistry, University of Buenos Aires, Junín 956 PB , Buenos Aires, Argentina.
F TesanLaboratory of Radioisotopes, School of Pharmacy and Biochemistry, University of Buenos Aires, Junín 956 PB , Buenos Aires, Argentina.
J C PerazzoDepartment of Pathophysiology, School of Pharmacy and Biochemistry, University of Buenos Aires , Buenos Aires, Argentina.
G A CremaschiLaboratory of Radioisotopes, School of Pharmacy and Biochemistry, University of Buenos Aires, Junín 956 PB, Buenos Aires, Argentina; Neuroimmunomodulation and Molecular Oncology Division, Institute for Biomedical Research (BIOMED), School of Medical Sciences, Pontifical Catholic University of Argentina (UCA), and the National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina.
E S RiveraLaboratory of Radioisotopes, School of Pharmacy and Biochemistry, University of Buenos Aires, Junín 956 PB , Buenos Aires, Argentina.
V A MedinaLaboratory of Radioisotopes, School of Pharmacy and Biochemistry, University of Buenos Aires, Junín 956 PB, Buenos Aires, Argentina; Laboratory of Cellular and Molecular Biology, Institute for Biomedical Research (BIOMED), School of Medical Sciences, Pontifical Catholic University of Argentina (UCA), and the National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina.
University of Buenos Aires · ARPontificia Universidad Católica Argentina · ARConsejo Nacional de Investigaciones Científicas y Técnicas · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present work was to evaluate the potential protective effect of histamine on Doxorubicin (Dox)-induced hepatic and cardiac toxicity in different rodent species and in a triple-negative breast tumor-bearing mice model. Male Sprague Dawley rats and Balb/c mice were divided into four groups: control (received saline), histamine (5 mg/kg for rats and 1 mg/kg for mice, daily subcutaneous injection starting 24 h before treatment with Dox), Dox (2 mg/kg, intraperitoneally injected three times a week for 2 weeks) and Dox+histamine (received both treatments). Tissue toxicity was evaluated by histopathological studies and oxidative stress and biochemical parameters. The combined effect of histamine and Dox was also investigated in vitro and in vivo in human MDA-MB-231 triple-negative breast cancer model. Heart and liver of Dox-treated animals displayed severe histological damage, loss of tissue weight, increased TBARS levels and DNA damage along with an augment in serum creatine kinase-myocardial band. Pretreatment with histamine prevented Dox-induced tissue events producing a significant preservation of the integrity of both rat and mouse myocardium and liver, through the reduction of Dox-induced oxidative stress and apoptosis. Histamine treatment preserved anti-tumor activity of Dox, exhibiting differential cytotoxicity and increasing the Dox-induced inhibition of breast tumor growth. Findings provide preclinical evidence indicating that histamine could be a promising candidate as a selective cytoprotective agent for the treatment of Dox-induced cardiac and hepatic toxicity, and encourage the translation to clinical practice.

Identifiers

PMID27551485
PMCPMC4979467
OpenAlexW2515965384

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.