ArticleInflammopharmacology2022
The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument.
Article in Inflammopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Ivabradine for the Prevention of Anthracycline-Induced Cardiotoxicity in Female Patients with Primarily Breast Cancer: A Prospective, Randomized, Open-Label Clinical Trial.Medicina (Kaunas, Lithuania) · 2023Trial
- Ivabradine as a Cardio-Protective Agent Against Anthracycline-Induced Cardiotoxicity: A Narrative Review.Cardiovascular drugs and therapy · 2026Review
- Ivabradine for anthracycline-induced cardiotoxicity: emerging promise and current evidence.Annals of medicine and surgery (2012) · 2026Article
- Targeting AMPK with ivabradine attenuates cyclophosphamide-induced hepatotoxicity: Crosstalk with MAPK, JAK1/STAT3, and PI3K/Akt pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Exploring the Neuroprotective Effects of Rufinamide in a Streptozotocin-Induced Dementia Model.Cellular and molecular neurobiology · 2024Article
- Management of Fluoropyrimidine-Induced Cardiac Adverse Outcomes Following Cancer Treatment.Cardiovascular toxicology · 2024Review
- Comparative effects of incretin-based therapy on doxorubicin-induced nephrotoxicity in rats: the role of SIRT1/Nrf2/NF-κB/TNF-α signaling pathways.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated the potential role of ivabradine (IVN) in the attenuation of doxorubicin (DXR)-induced cardiotoxicity in rats. A total of 28 Swiss-Albino male mice were used, divided into four equal groups: the negative control did not receive any agents (n = 7), the DXR group received a single dose of DXR 20 mg/kg (n = 7), the treated group A was pretreated with IVN 5 mg/kg plus DXR (n = 7), and the treated group B was pretreated with IVN 10 mg/kg plus DXR (n = 7). The duration of this study was 10 days. Inflammatory biomarkers, including tumor necrosis factor alpha (TNF-α), lactate dehydrogenase (LDH), malondialdehyde (MDA), and cardiac troponin (cTn-I) serum levels were measured. TNF-α, LDH, MDA, and cTn-I serum levels were higher in the DXR-treated mice compared with the control (P˂0.01). IVN produced a dose-dependent effect in the reduction of MDA and cTn-I compared to DXR-treated mice (P˂0.05). Our findings suggest that IVN is an effective agent in mitigating DXR-induced cardiotoxicity due to its anti-inflammatory and antioxidant effects. IVN illustrated a dose-dependent effect in the attenuation of DXR-induced cardiotoxicity through inhibition of lipid peroxidation and cardiomyocyte injury.
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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 Socratic graph.