ArticleFrontiers in pharmacology2020
The Prophylactic Effect of Pinocembrin Against Doxorubicin-Induced Cardiotoxicity in an
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Dysfunctional high-density lipoprotein particles are associated with cardiac alterations in cancer patients and tumor-bearing mice receiving doxorubicin.Basic research in cardiology · 2026Article
- Antitumor natural products targeting mitochondrial NADH: ubiquinone oxidoreductase (complex I): a review.Frontiers in pharmacology · 2026Review
- Downregulation of Alox5 Inhibits Ferroptosis to Improve Doxorubicin-Induced Cardiotoxicity via the P53/SLC7A11 Pathway.Journal of cellular and molecular medicine · 2025Article
- In Vitro Evaluation of the Safety and Antineoplastic Effects in Gastrointestinal Tumors of Nanostructured Lipid Carriers Loaded with Berberine.Pharmaceutics · 2025Article
- Design, synthesis and biological evaluation of buthutin derivatives as cardioprotective agents.Natural products and bioprospecting · 2025Article
- Doxorubicin-Induced Cardiomyopathy: A Preliminary Study on the Cardioprotective Benefits of 7-Hydroxyflavanone.International journal of molecular sciences · 2023Article
- Review
- Pinocembrin Inhibits P2X4 Receptor-Mediated Pyroptosis in Hippocampus to Alleviate the Behaviours of Chronic Pain and Depression Comorbidity in Rats.Molecular neurobiology · 2022Article
- Wogonin reduces cardiomyocyte apoptosis from mitochondrial release of cytochromeExperimental and therapeutic medicine · 2022Article
- Breviscapine remodels myocardial glucose and lipid metabolism by regulating serotonin to alleviate doxorubicin-induced cardiotoxicity.Frontiers in pharmacology · 2022Article
- Nicotinic Acid Riboside Regulates Nrf-2/P62-Related Oxidative Stress and Autophagy to Attenuate Doxorubicin-Induced Cardiomyocyte Injury.BioMed research international · 2022Review
- Cariporide Attenuates Doxorubicin-Induced Cardiotoxicity in Rats by Inhibiting Oxidative Stress, Inflammation and Apoptosis Partly Through Regulation of Akt/GSK-3β and Sirt1 Signaling Pathway.Frontiers in pharmacology · 2022Article
- Prevention of Anthracycline-Induced Cardiotoxicity: The Good and Bad of Current and Alternative Therapies.Frontiers in cardiovascular medicine · 2022Review
- Article
- The Implication of Low Dose Dimethyl Sulfoxide on Mitochondrial Function and Oxidative Damage in Cultured Cardiac and Cancer Cells.Molecules (Basel, Switzerland) · 2021Article
- Pinocembrin ameliorates post-infarct heart failure through activation of Nrf2/HO-1 signaling pathway.Molecular medicine (Cambridge, Mass.) · 2021Article
- Chlorogenic Acid Enhances Doxorubicin-Mediated Cytotoxic Effect in Osteosarcoma Cells.International journal of molecular sciences · 2021Article
- Mechanisms of anthracycline-mediated cardiotoxicity and preventative strategies in women with breast cancer.Molecular and cellular biochemistry · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe clinical use of Doxorubicin (Dox) is significantly limited by its dose-dependent cardiotoxic side effect. Accumulative evidence suggests that the use of flavonoids, such as the antioxidative Pinocembrin (Pin), could be effective in the prevention of Dox-induced cardiotoxicity. Accordingly, we investigated the ability of pinocembrin (Pin) to attenuate Dox-induced cardiotoxicity in an in vitro H9c2 cardiomyoblast model. METHODOLOGY: The cardioprotective potential of Pin was established in H9c2 cells. Here, cells were treated with Dox (2μM), Dox (2μM) + Pin (1μM), and Dox (2μM) + Dexrazoxane (20μM) for 6 days. Thereafter, the safe co-administration of Pin with Dox, in a cancer environment, was investigated in MCF-7 breast cancer cells subjected to the same experimental conditions. Untreated cells served as the control. Subsequently, Pin's ability to attenuate Dox-mediated oxidative stress, impaired mitochondrial bioenergetics and potential, as well as aggravated apoptosis was quantified using biochemical assays.
resultsThe results demonstrated that co-treatment with Pin mitigates Dox-induced oxidative stress by alleviating the antioxidant enzyme activity of the H9c2 cells. Pin further reduced the rate of apoptosis and necrosis inferred by Dox by improving mitochondrial bioenergetics. Interestingly, Pin did not decrease the efficacy of Dox but, rather increased the rate of apoptosis and necrosis in Dox-treated MCF-7 cells.
conclusionThe findings presented in this study showed, for the first time, that Pin attenuates Dox-induced cardiotoxicity without reducing its chemotherapeutic effect. We propose that additional studies, using in vivo models, should be conducted to further investigate Pin as a suitable candidate in the prevention of the cardiovascular dysfunction inferred by Dox administration.
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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.