Evidence map›Paper›PMID 26091236›Full record

ArticleNutrients2015

In Vivo Protective Effects of Diosgenin against Doxorubicin-Induced Cardiotoxicity.

Chih-Tai Chen, Zhi-Hong Wang, Cheng-Chin Hsu, Hui-Hsuan Lin, Jing-Hsien Chen

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Diosgenin ameliorates silica-induced tuberculosis in rats.Animal models and experimental medicine · 2025
    Article
  5. Review
  6. Article
  7. Sage (Anatomy & cell biology · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Secondary Metabolites, Antioxidant, and Antiproliferative Activities ofEvidence-based complementary and alternative medicine : eCAM · 2021
    Article
  20. Review
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.

Chih-Tai ChenSchool of Nutrition, Chung Shan Medical University, Taichung City 40201, Taiwan. thomas.chen@unitybiotech.com.
Zhi-Hong WangEnvironment-Omics-Diseases Research Center, China Medical University Hospital, Taichung City 40402, Taiwan. rover_wang@hotmail.com.
Cheng-Chin HsuSchool of Nutrition, Chung Shan Medical University, Taichung City 40201, Taiwan. king@csmu.edu.tw.
Hui-Hsuan LinSchool of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung City 40201, Taiwan. linhh@csmu.edu.tw.
Jing-Hsien ChenSchool of Nutrition, Chung Shan Medical University, Taichung City 40201, Taiwan. cjh0828@csmu.edu.tw.
Chung Shan Medical University · TWChina Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doxorubicin (DOX) induces oxidative stress leading to cardiotoxicity. Diosgenin, a steroidal saponin of Dioscorea opposita, has been reported to have antioxidant activity. Our study was aimed to find out the protective effect of diosgenin against DOX-induced cardiotoxicity in mice. DOX treatment led to a significant decrease in the ratio of heart weight to body weight, and increases in the blood pressure and the serum levels of lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and creatine kinase myocardial bound (CK-MB), markers of cardiotoxicity. In the heart tissue of the DOX-treated mice, DOX reduced activities of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GPx), were recovered by diosgenin. Diosgenin also decreased the serum levels of cardiotoxicity markers, cardiac levels of thiobarbituric acid relative substances (TBARS) and reactive oxygen species (ROS), caspase-3 activation, and mitochondrial dysfunction, as well as the expression of nuclear factor kappa B (NF-κB), an inflammatory factor. Moreover, diosgenin had the effects of increasing the cardiac levels of cGMP via modulation of phosphodiesterase-5 (PDE5) activity, and in improving myocardial fibrosis in the DOX-treated mice. Molecular data showed that the protective effects of diosgenin might be mediated via regulation of protein kinase A (PKA) and p38. Our data imply that diosgenin possesses antioxidant and anti-apoptotic activities, and cGMP modulation effect, which in turn protect the heart from the DOX-induced cardiotoxicity.

Indexed as

AnimalsAntioxidantsApoptosisBiomarkersBlood PressureCardiomyopathiesCardiotoxicityCaspase 3Creatine KinaseDioscoreaDiosgeninDoxorubicinGlutathione PeroxidaseHeart RateL-Lactate DehydrogenaseMaleAntioxidantsBiomarkersCasp3 protein, mouseCaspase 3Creatine KinaseDiosgeninDoxorubicinGlutathione PeroxidaseL-Lactate DehydrogenasePlant ExtractsReactive Oxygen SpeciesSuperoxide DismutaseThiobarbituric Acid Reactive SubstancesantioxidantcadiotoxicitycGMPdiosgenindoxorubicin

Identifiers

PMID26091236
PMCPMC4488824
OpenAlexW2144567633

What OpenQuestion holds

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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.