Evidence map›Paper›PMID 32172286›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2020

Curcumin attenuates bevacizumab-induced toxicity via suppressing oxidative stress and preventing mitochondrial dysfunction in heart mitochondria.

Nima Shokouhi Sabet, Saman Atashbar, Elham Mohammad Khanlou, Farzad Kahrizi, Ahmad Salimi

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  13. Cardio-Oncology: Mechanisms, Drug Combinations, and Reverse Cardio-Oncology.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Prohibitins: A Key Link between Mitochondria and Nervous System Diseases.Oxidative medicine and cellular longevity · 2022
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Bevacizumab induces oxidative cytotoxicity and apoptosis via TRPM2 channel activation in retinal pigment epithelial cells: Protective role of glutathione.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2021
    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

5 authors at 2 institutions in 1 country.

Nima Shokouhi SabetDepartment of Pharmacology and Toxicology, School of Pharmacy, Ardabil University of Medical Sciences, P.O. Box: 56189-53141, Ardabil, Iran.
Saman AtashbarDepartment of Pharmacology and Toxicology, School of Pharmacy, Ardabil University of Medical Sciences, P.O. Box: 56189-53141, Ardabil, Iran.
Elham Mohammad KhanlouDepartment of Pharmacology and Toxicology, School of Pharmacy, Ardabil University of Medical Sciences, P.O. Box: 56189-53141, Ardabil, Iran.
Farzad KahriziDepartment of Toxicology and Pharmacology, Faculty of Pharmacy, Damghan Islamic Azad University, Damghan, Iran.
Ahmad SalimiDepartment of Pharmacology and Toxicology, School of Pharmacy, Ardabil University of Medical Sciences, P.O. Box: 56189-53141, Ardabil, Iran. salimikd@yahoo.com.
Ardabil University of Medical Sciences · IRIslamic Azad University, Damghan Branch · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure was subsequently noted in 2-4% of patients on bevacizumab (BEV). Whereas mitochondria play an important role in myocardial tissue homeostasis, deterioration in mitochondrial function will eventually lead to cardiomyocyte cell death and consequently cardiovascular dysfunction. Therefore, the aim of our study is to search the effects of BEV on isolated rat heart mitochondria and cardiomyocytes, and survey the effect of curcumin as a mitochondrial protective and cardioprotective agent. Rat heart mitochondria and cardiomyocytes were isolated from adult rat heart ventricular. By using biochemical and flow cytometry evaluations, the parameters of mitochondrial toxicity including succinate dehydrogenase (SDH) activity, mitochondrial swelling, mitochondrial membrane potential (MMP) collapse, reactive oxygen species (ROS) formation and lipid peroxidation (LP), and cellular assays such as cytotoxicity and MMP collapse were evaluated. Results revealed that BEV (up to 50 μg/ml) induced a concentration- and time-dependent rise in mitochondrial ROS formation, MMP collapse, mitochondrial swelling, LP, and inhibition of SDH in rat heart mitochondria. Our results showed that curcumin (10-100 μM) significantly ameliorated BEV-induced mitochondrial toxicities. Also, our results in cellular assays confirmed amelioration effect of curcumin against BEV toxicity. These results indicate that the cardiotoxic effects of BEV are associated with mitochondrial dysfunction and ROS formation, which finally ends in MMP collapse and mitochondrial swelling as the "point of no return" in the cascade of events leading to apoptosis. Also, results of this study suggest that probably the combination therapy of BEV and curcumin could decrease mitochondrial effects of this drug.

Indexed as

Angiogenesis InhibitorsAnimalsAntioxidantsApoptosisBevacizumabCardiotoxicityCurcuminHeart FailureLipid PeroxidationMaleMembrane Potential, MitochondrialMitochondria, HeartMitochondrial SwellingMyocytes, CardiacOxidative StressRats, WistarAngiogenesis InhibitorsAntioxidantsBevacizumabCurcuminReactive Oxygen SpeciesCardioprotectiveCardiotoxicityHeart failureMitochondria

Identifiers

PMID32172286
OpenAlexW3012079952

What OpenQuestion holds

Textmetadata
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.