Mitigating Doxorubicin-Induced Cardiotoxicity: Insights into the Therapeutic Potential of Raspberry Ketone

Document Type : Mini-reviews

Authors

1 Pharmacology and Toxicology department, faculty of pharmacy, Port said university

2 pharmacology and toxicology department , Faculty of pharmacy, Suez canal university

3 pharmacology and toxicology department, Faculty of pharmacy, port said university

4 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Suez Canal University

10.21608/rpbs.2025.386242.1373

Abstract

Doxorubicin (DOX), an anthracycline antibiotic, remains a cornerstone in the management of a wide spectrum of malignancies due to its high antitumor efficacy. Its use, however, is severely limited by dose-dependent and cumulative cardiotoxicity, which can result in irreversible heart failure. The pathophysiology of DOX-induced cardiotoxicity is complex and multifactorial, involving oxidative stress, mitochondrial dysfunction, iron-mediated injury, apoptosis, inflammation, and fibrotic remodeling. Emerging evidence indicates that impairment of the nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway plays a pivotal role in exacerbating cardiac susceptibility to DOX-induced injury. The identification of pharmacological strategies that can restore Nrf2 function has therefore become a priority. Raspberry ketone (RK), a naturally occurring phenolic compound found predominantly in red raspberries, exhibits potent antioxidant, anti-inflammatory, metabolic regulatory, hepatoprotective, neuroprotective, and dermatological benefits. Several studies suggest that RK may modulate Nrf2 signaling, thereby enhancing the antioxidant defense system and attenuating oxidative damage. This review comprehensively discusses the DOX-induced cardiotoxicity and the cardioprotective potential of RK through its Nrf2-modulating properties.

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