ArticleRedox biology2018
Protective effect of dioscin against doxorubicin-induced cardiotoxicity via adjusting microRNA-140-5p-mediated myocardial oxidative stress.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed.
- MicroRNAs and Alarmins in Cardio-Oncology: Biomarkers and Therapeutic Implications in Skin and Breast Cancer.International journal of molecular sciences · 2026Review
- Inhibiting NLPR3 inflammasome by FOXO3-mediated activation of SIRT2 alleviates myocardial injury in rats.Histology and histopathology · 2026Article
- Research Progress on the Role of Traditional Chinese Medicine in Regulating Ferroptosis in Cardiovascular Diseases.Biology · 2026Review
- Targeting miR-144-5p/ACSM1 Axis Alleviates Doxorubicin-Induced Heart Failure by Inhibiting Lipid Peroxidation.Current medical science · 2025Article
- Mild Drought Promotes Biomass Accumulation and Increases Diosgenin Content in Rhizomes ofPlants (Basel, Switzerland) · 2025Article
- The Role of miRNAs in Chemotherapy-Induced Cardiotoxicity.Biomedicines · 2025Review
- A recent decade update on combating doxorubicin-induced toxicities.Archives of toxicology · 2025Review
- Natural products targeting regulated cell deaths for adriamycin-induced cardiotoxicity.Cell death discovery · 2025Review
- Cardioprotective potential of protocatechuic acid against doxorubicin-induced cardiotoxicity in rats.Research in pharmaceutical sciences · 2025Article
- The role and mechanism of epigenetics in anticancer drug-induced cardiotoxicity.Basic research in cardiology · 2025Review
- Deciphering Oxidative Stress in Cardiovascular Disease Progression: A Blueprint for Mechanistic Understanding and Therapeutic Innovation.Antioxidants (Basel, Switzerland) · 2024Review
- Sarmentosin alleviates doxorubicin-induced cardiotoxicity and ferroptosisRedox report : communications in free radical research · 2024Article
- Transforming Cardiotoxicity Detection in Cancer Therapies: The Promise of MicroRNAs as Precision Biomarkers.International journal of molecular sciences · 2024Review
- CaMKII Exacerbates Doxorubicin-Induced Cardiotoxicity by Promoting Ubiquitination Through USP10 Inhibition.Cancer medicine · 2024Article
- NOX1-mediated oxidative stress induces chondrocyte ferroptosis by inhibiting the Nrf2/HO-1 pathway.Scientific reports · 2024Article
- Hepatoprotective efficacy ofOpen veterinary journal · 2024Article
- Article
- Prophylactic impacts ofOpen veterinary journal · 2024Article
- Role of diosmin in preventing doxorubicin-induced cardiac oxidative stress, inflammation, and hypertrophy: A mechanistic approach.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- Food therapy of scutellarein ameliorates pirarubicin‑induced cardiotoxicity in rats by inhibiting apoptosis and ferroptosis through regulation of NOX2‑induced oxidative stress.Molecular medicine reports · 2024Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinical application of doxorubicin (DOX) is limited because of its cardiotoxicity. Thus, exploration of effective lead compounds against DOX-induced cardiotoxicity is necessary. The aim of the present study was to investigate the effects and possible mechanisms of dioscin against DOX-induced cardiotoxicity. The in vitro model of DOX- treated H9C2 cells and the in vivo models of DOX-treated rats and mice were used in this study. The results showed that discoin markedly increased H9C2 cell viability, decreased the levels of CK, LDH, and improved histopathological and electrocardio- gram changes in rats and mice to protect DOX-induced cardiotoxicity. Furthermore, dioscin significantly inhibited myocardial oxidative insult through adjusting the levels of intracellular ROS, MDA, SOD, GSH and GSH-Px in vitro and in vivo. Our data also indicated that dioscin activated Nrf2 and Sirt2 signaling pathways, and thereby affected the expression levels of HO-1, NQO1, Gst, GCLM, Keap1 and FOXO3a through decreasing miR-140-5p expression level. In addition, the level of intracellular ROS was significantly increased in H9C2 cells treated by DOX after miR-140-5p mimic transfection, as well as the down-regulated expression levels of Nrf2 and Sirt2, which were markedly reversed by dioscin. In conclusion, our data suggested that dioscin alleviated DOX-induced cardiotoxicity through modulating miR-140-5p-mediated myocardial oxidative stress. This natural product should be developed as a new candidate to alleviate cardiotoxicity caused by DOX in the future.
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