Affiliations 

  • 1 Department of Chemical Sciences, Faculty of Science and Technology, Universiti Kebangsaan Malaysia, UKM, 43600, Bangi, Selangor, Malaysia
  • 2 Programme of Biomedical Science, Centre for Toxicology and Health Risk Studies (CORE), Faculty of Health Sciences, Universiti Kebangsaan Malaysia, 50300, Kuala Lumpur, Malaysia
  • 3 Faculty of Pharmacy, Drug and Herbal Research Centre, Universiti Kebangsaan Malaysia, 50300, Kuala Lumpur, Malaysia
  • 4 Department of Physiology, Faculty of Medicine, Universiti Kebangsaan Malaysia, 56000, Kuala Lumpur, Malaysia
  • 5 International Joint Department of Materials Science and Engineering Between National University of Malaysia and Gifu University, Graduate School of Engineering, Gifu University, 1-1 Yanagido, Gifu, 501-1193, Japan
  • 6 Programme of Biomedical Science, Centre for Toxicology and Health Risk Studies (CORE), Faculty of Health Sciences, Universiti Kebangsaan Malaysia, 50300, Kuala Lumpur, Malaysia. satirah@ukm.edu.my
  • 7 Department of Chemical Sciences, Faculty of Science and Technology, Universiti Kebangsaan Malaysia, UKM, 43600, Bangi, Selangor, Malaysia. jalifah@ukm.edu.my
Cardiovasc Toxicol, 2024 Nov 26.
PMID: 39592525 DOI: 10.1007/s12012-024-09940-8

Abstract

Doxorubicin (DOX) is a remarkable chemotherapeutic agent, however, its adverse effect on DOX-induced cardiotoxicity (DIC) is a rising concern. Recent research has identified carvacrol (CAR), an antioxidant and anti-inflammatory agent, as a promising natural compound for protecting against DIC. This study aims to investigate the potential cardioprotective effects properties of CAR in vitro and in vivo. The cardioprotective effect of CAR was assessed by pretreating H9c2 cells with non-toxic CAR for 24 h, followed by co-treatment with DOX (10 μM) for an additional 24 h. The cell viability was determined using an MTT assay. For the in vivo study, male Sprague-Dawley rats (200-250 g) were randomly divided into three groups: control, cardiotoxicity (DOX), and treatment (CAR + DOX) groups. CAR (50 mg/kg, BW) was administered orally to the CAR + DOX groups for 14 days. Then, a single dose of DOX (15 mg/kg/i.p, BW) was administered on day 15 for DOX and CAR + DOX groups. The rats were allowed to recover for 3 days before being sacrificed. Our results demonstrated that DOX (10 µM) significantly reduced H9c2 cell viability by 50% (p 

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.