ArticleMolecular medicine reports2017
Naringin protects myocardial cells from doxorubicin‑induced apoptosis partially by inhibiting the p38MAPK pathway.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Pooled it
- Nutritional Prevention of Oxidative Stress-Induced Cardiotoxicity in Pediatric Cardio-Oncology: Molecular Mechanisms and Translational Perspectives-A Narrative Review.International journal of molecular sciences · 2026Review
- Research Progress on the Role of Traditional Chinese Medicine in Regulating Ferroptosis in Cardiovascular Diseases.Biology · 2026Review
- Osthole attenuates trastuzumab-induced cardiotoxicity in mice by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway.Journal of traditional and complementary medicine · 2026Article
- Naringin regulates the cGAS-STING pathway to improve mitochondrial dysfunction and ferroptosis after myocardial ischemia-reperfusion injury.Cytotechnology · 2025Article
- Natural products targeting regulated cell deaths for adriamycin-induced cardiotoxicity.Cell death discovery · 2025Review
- Mechanistic Insights into Flavonoid Subclasses as Cardioprotective Agents Against Doxorubicin-Induced Cardiotoxicity: A Comprehensive Review.Drug design, development and therapy · 2025Review
- The potential of flavonoids to mitigate cellular senescence in cardiovascular disease.Biogerontology · 2024Review
- Unveiling the power of flavonoids: A dynamic exploration of their impact on cancer through matrix metalloproteinases regulation.BioMedicine · 2024Review
- Naringin attenuates acute myocardial ischemia-reperfusion injury via miR- 126/GSK-3β/β-catenin signaling pathway.Acta cirurgica brasileira · 2022Article
- Naringin Interferes Doxorubicin-Induced Myocardial Injury by Promoting the Expression of ECHS1.Frontiers in pharmacology · 2022Article
- Naringin attenuates rat myocardial ischemia/reperfusion injury via PI3K/Akt pathway-mediated inhibition of apoptosis, oxidative stress and autophagy.Experimental and therapeutic medicine · 2021Article
- Astragaloside IV ameliorates endoplasmic reticulum stress‑induced apoptosis of Aβ25‑35‑treated PC12 cells by inhibiting the p38 MAPK signaling pathway.Molecular medicine reports · 2019Article
- Mitochondria-Targeting Small Molecules Effectively Prevent Cardiotoxicity Induced by Doxorubicin.Molecules (Basel, Switzerland) · 2018Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX) has been widely used to treat cancers as a first‑line antitumor drug. However, it causes severe, irreversible, dose‑dependent cardiotoxicity. To evaluate the protective effects of naringin (NRG) on cardiotoxicity, the authors investigated the molecular mechanism of the p38MAPK signaling pathway. H9c2 cells were treated for 24 h by using 5 µmol/l DOX without or with being pretreated by 1 µM NRG for 150 min or by 3 µM SB203580 for 60 min. Cell viability was detected by cell counting kit‑8 assay. Intracellular reactive oxygen species (ROS) levels were detected based on the oxidative conversion of 2',7'‑dichlorfluorescein‑diacetate (cell‑permeable) to dichlorofluorescein (fluorescent). The expression of p38MAPK was determined by western blotting. The expression level of p‑p38MAPK in H9c2 cells, which was significantly increased by exposure to 5 µM DOX for 60 min (P<0.01), was significantly decreased by pretreatment with 1 µM NRG for 150 min beforehand (P<0.01). The viability of H9c2 cells pretreated for 150 min with 1 µM NRG was significantly enhanced compared with that using DOX directly (P<0.01). Intracellular ROS levels were significantly reduced by being pretreated with 1 µM NRG for 150 min or with 3 µM SB203580 for 60 min before the cells were exposed to 5 µM DOX. Collectively, NRG protected H9c2 cells against the cardiotoxicity induced by DOX through suppressing the expression and activity of the p38MAPK pathway. The findings provided valuable evidence for the possible use of NRG to relieve DOX‑induced cardiotoxicity.
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