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Maha Abdullah Alwaili,1 Abdallah H Elhoby,2 Norhan M El-Sayed,2 Islam Z Mahmoud,3 Afaf Alharthi,4 Mohammad El-Nablaway,5,6 Dina M Khodeer2 1Department of Biology, College of Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia; 2Department of Pharmacology and Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia, Egypt; 3Department of Cardiovascular Medicine, Faculty of Medicine, Suez Canal University, Ismailia, Egypt; 4Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, Taif, Saudi Arabia; 5Department of Basic Medical Sciences, College of Medicine, AlMaarefa University, Diriyah, Riyadh, 13713, Saudi Arabia; 6Department of Medical Biochemistry, Faculty of Medicine, Mansoura University, Mansoura, 35516, EgyptCorrespondence: Dina M Khodeer, Email dina_khoudaer@pharm.suez.edu.egIntroduction: This comprehensive study investigated the therapeutic potential of α-asarone in mitigating myocardial oxidative damage, primarily induced by hexavalent chromium (Cr(VI)) exposure in mice.Methods: In this experiment, 24 mice were divided into four groups to assess the cardioprotective role of α-asarone. The study focused on two treatment groups, receiving 25 mg and 50 mg of α-asarone, respectively. These groups were compared against a control group subjected to Cr(VI) without α-asarone treatment, and a normal control negative group. The key biochemical parameters evaluated included serum levels of Creatine Kinase-MB (CK-MB) and Troponin I, markers indicative of myocardial damage. Additionally, the levels of Malondialdehyde (MDA) were measured to assess lipid peroxidation, alongside the evaluation of key inflammatory biomarkers in cardiac tissue homogenates, such as Tumor Necrosis Factor-α (TNF-α) and Interleukin-1β (IL-1β). Results Remarkably, α-asarone treatment resulted in a significant reduction in these markers compared to the control group. The treatment also elevated the activity of cardinal antioxidant enzymes like catalase (CAT) and superoxide dismutase (SOD), and reduced the glutathione (GSH). Furthermore, a notable upregulation of Peroxisome Proliferator-Activated Receptor Gamma (PPAR-γ) in cardiac tissue homogenates was observed, highlighting a potential pathway through which α-asarone exerts its protective effects. Histopathological analysis of cardiac tissues revealed that α-asarone ameliorated the structural lesions induced by Cr(VI). The study thus provides substantial evidence that α-asarone ameliorates Cr(VI)-induced cardiotoxicity through a multifaceted approach. It enhances cardiac enzyme function, modulates free radical generation, improves antioxidant status, and mitigates histopathological damage in cardiac tissues. Given these findings, α-asarone emerges as a promising agent against Cr(VI)-induced myocardial injury.Purpose: This study paves the way for further research into the cardioprotective properties of α-asarone and its potential application in clinical settings by specifically exploring the protective efficacy of α-asarone against Cr(VI)-induced cardiotoxicity and delineating the underlying biochemical and molecular mechanisms involved.Keywords: α-asarone, chromium, mice, cardiotoxicity, oxidative stress, histopathological studies