Evidence map›Paper›PMID 27446329›Full record

ArticleExperimental and therapeutic medicine2016

Resveratrol inhibits doxorubicin-induced cardiotoxicity via sirtuin 1 activation in H9c2 cardiomyocytes.

Mi-Hua Liu, Jian Shan, Jian Li, Yuan Zhang, Xiao-Long Lin

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Novel Therapeutics for Anthracycline Induced Cardiotoxicity.Frontiers in cardiovascular medicine · 2022
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. CYP1B1 as a therapeutic target in cardio-oncology.Clinical science (London, England : 1979) · 2020
    Article
  18. Review
  19. 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

5 authors at 5 institutions in 1 country.

Mi-Hua LiuDepartment of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
Jian ShanDepartment of Pathology, Zhongshan Torch Development Zone Hospital, Zhongshan, Guangdong 528437, P.R. China.
Jian LiDepartment of Ultrasonic Diagnosis, Bo'Ai Hospital of Zhongshan, Zhongshan, Guangdong 528403, P.R. China.
Yuan ZhangDepartment of Pathology, Mawangdui Hospital, Changsha, Hunan 410016, P.R. China.
Xiao-Long LinDepartment of Pathology, The Third People's Hospital of Huizhou, Affiliated Huizhou Hospital of Guangzhou Medical University, Huizhou, Guangdong 516002, P.R. China.
Boai Hospital of Zhongshan · CNGuangzhou Development Zone Hospital · CNGuangzhou Medical University · CNHunan Mawangdui Hospital · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doxorubicin (DOX) is an efficient drug used in cancer therapy; however, it can induce severe cytotoxicity, which limits its clinical application. In the present study, the effects of resveratrol (RES) on sirtuin 1 (SIRT1) activation in mediating DOX-induced cytotoxicity in H9c2 cardiac cells was investigated. H9c2 cells were exposed to 5 µM DOX for 24 h to establish a model of DOX cardiotoxicity. Apoptosis of H9c2 cardiomyocytes was assessed using the MTT assay and Hoechst nuclear staining. The results demonstrated that pretreating H9c2 cells with RES prior to the exposure of DOX resulted in increased cell viability and a decreased quantity of apoptotic cells. Western blot analysis demonstrated that DOX decreased the expression level of SIRT1. These effects were significantly alleviated by co-treatment with RES. In addition, the results demonstrated that DOX administration amplified forkhead box O1 (FoxO1) and P53 expression levels in H9c2 cells. RES was also found to protect against DOX-induced increases of FoxO1 and P53 expression levels in H9c2 cells. Furthermore, the protective effects of RES were arrested by the SIRT1 inhibitor nicotinamide. In conclusion, the results demonstrated that RES protected H9c2 cells against DOX-induced injuries via SIRT1 activation.

Indexed as

apoptosisdoxorubicinforkhead box protein O1resveratrolsirtuin 1

Identifiers

PMID27446329
PMCPMC4950526
OpenAlexW2417571213

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.