ArticleExperimental and therapeutic medicine2018
Glibenclamide exacerbates adriamycin-induced cardiotoxicity by activating oxidative stress-induced endoplasmic reticulum stress in rats.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 4 papers.
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4 citing papers in PubMed, 11 citations in OpenAlex.
- Anti-Diabetic Therapies and Cancer: From Bench to Bedside.Biomolecules · 2024Review
- Identification of Dalbergiae Odoriferae Lignum active ingredients and potential mechanisms in the treatment of adriamycin-induced cardiotoxicity based on network pharmacology and experimental verification.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Ameliorative effects ofSaudi journal of biological sciences · 2022Article
- Protective Effect and Mechanism of Bone Morphogenetic Protein-4 on Apoptosis of Human Lens Epithelium Cells under Oxidative Stress.BioMed research international · 2021Article
Corrections and comments
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5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Adriamycin (ADR) is a chemotherapeutic drug used to treat tumors in a clinical setting. However, its use is limited by a side effect of cardiotoxicity. Glibenclamide (Gli), an inhibitor of mitochondrial ATP-dependent potassium (K-ATP) channels, blocks the cardioprotective effects of mitochondrial K-ATP channel openers and induces apoptosis in rodent pancreatic islet β-cell lines. However, little is known about the role of Gli in ADR-induced cardiotoxicity. The present study was designed to investigate the impact of Gli on ADR-induced cardiotoxicity in rats. A total of 60 male Sprague-Dawley rats were divided into the following 4 groups: i) Control; ii) Gli; iii) ADR; and iv) Gli+ADR (n=15 in each). The rats in the ADR and Gli+ADR groups were treated with ADR (intraperitoneal, 2.5 mg/kg/week) for 6 weeks. The rats in the Gli and Gli+ADR groups received Gli at a dose of 12 mg/kg/day via gastric lavage for 30 days from the eighth week of the study. Following the completion of Gli treatment, cardiac function was assessed by echocardiography, and the rats were sacrificed. The hearts were subsequently harvested for analysis. The rats in the ADR group demonstrated significantly impaired cardiac function and increased levels of oxidative stress, endoplasmic reticulum stress (ERS) and apoptosis in the heart compared with rats in the control and Gli groups (without ADR treatment). These abnormalities were exacerbated by Gli in the Gli+ADR group. Gli treatment decreased cardiac function and significantly increased oxidative stress, ERS and apoptosis levels in myocardial tissues in rats treated with ADR. The findings indicated that Gli triggers oxidative stress-induced ERS, and thus exacerbates ADR-induced cardiotoxicity in rats.
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