Evidence map›Paper›PMID 39827225›Full record

ArticleCardiovascular toxicology2025

Taxifolin Protects Against 5-Fluorouracil-Induced Cardiotoxicity in Mice Through Mitigating Oxidative Stress, Inflammation, and Apoptosis: Possible Involvement of Sirt1/Nrf2/HO-1 Signaling.

Mohammad H Abukhalil, Zina Al-Alami, Manal A Alfwuaires, Mohd Rasheeduddin Imran, Saleem H Aladaileh, Osama Y Althunibat

Abstract read
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In one paragraph

Article in Cardiovascular toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Potential role of SIRT1 in cell ferroptosis.Frontiers in cell and developmental biology · 2025
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

6 authors.

Mohammad H AbukhalilDepartment of Medical Analysis, Princess Aisha Bint Al-Hussein College of Nursing and Health Sciences, Al-Hussein Bin Talal University, Ma'an, 71111, Jordan. mabukhalil@ahu.edu.jo.ORCID 0000-0002-4018-6925
Zina Al-AlamiDepartment of Basic Medical Sciences, Faculty of Allied Medical Sciences, Al-Ahliyya Amman University, Amman, 19328, Jordan.
Manal A AlfwuairesDepartment of Biological Sciences, Faculty of Science, King Faisal University, 31982, Al-Ahsa, Saudi Arabia.
Mohd Rasheeduddin ImranDepartment of Pharmacy Practice, College of Pharmacy, University of Hafr Al Batin, 39553, Hafr Al Batin, Saudi Arabia.
Saleem H AladailehDepartment of Pharmacy Practice, College of Pharmacy, University of Hafr Al Batin, 39553, Hafr Al Batin, Saudi Arabia.
Osama Y AlthunibatDepartment of Medical Analysis, Princess Aisha Bint Al-Hussein College of Nursing and Health Sciences, Al-Hussein Bin Talal University, Ma'an, 71111, Jordan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although 5-fluorouracil (5-FU) is widely utilized in cancer treatment, its side effects, including cardiotoxicity, limit its use. Taxifolin (TAX) is a bioactive anti-inflammatory and antioxidant flavonoid. This study aimed to elucidate the protective effect of TAX against 5-FU-induced cardiac injury in male mice. Mice were treated with TAX (25 and 50 mg/kg, orally) for 10 days and a single dose of 150 mg/kg 5-FU at day 8. Mice intoxicated with 5-FU showed increased creatine kinase-MB and lactate dehydrogenase activities and troponin I levels, with multiple cardiac histopathological changes. They also showed a significant increase in cardiac malondialdehyde (MDA) and nitric oxide (NO) and decreases in myocardial reduced glutathione (GSH) content and superoxide dismutase (SOD) and catalase (CAT) activities (P < 0.001). Pretreatment of 5-FU-injected mice with TAX suppressed cardiac injury, decreased MDA and NO contents (P < 0.001), and boosted antioxidant defenses in the myocardium. Moreover, TAX attenuated cardiac inflammatory response, as evidenced by the decreased expression levels of cardiac NF-κB p65, inducible nitric oxide synthase (iNOS), and pro-inflammatory cytokines (P < 0.001). Largely, TAX ameliorated the decrease in Bcl-2 expression and the increase in BAX and caspase-3 in the heart. It also restored the cardiac Sirt1/Nrf2/HO-1 signaling pathway. In conclusion, TAX showed significant cardioprotective effects on 5-FU-induced cardiac injury and might represent a promising adjuvant in preventing cardiac injury associated with oxidative stress and inflammation.

Indexed as

Anti-Inflammatory AgentsAntioxidantsApoptosisFluorouracilHeart DiseasesHeme Oxygenase (Decyclizing)Inflammation MediatorsMembrane ProteinsMyocytes, CardiacNF-E2-Related Factor 2Oxidative StressQuercetinSirtuin 1AnimalsCardiotoxicityDisease Models, AnimalAnti-Inflammatory AgentsAntioxidantsFluorouracilHeme Oxygenase-1Heme Oxygenase (Decyclizing)Hmox1 protein, mouseInflammation MediatorsMembrane ProteinsNfe2l2 protein, mouseNF-E2-Related Factor 2QuercetinSirt1 protein, mouseSirtuin 1taxifolin5‐fluorouracilAnticancer chemotherapyCardiotoxicityNrf2Sirt1Taxifolin

Identifiers

What Socratic 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 Socratic graph.