Key result
Hesperidin mitigates cisplatin-induced cardiotoxicity in rats by restoring antioxidant defenses and regulating autophagy.
Why the study?
Cisplatin use is limited by cardiac toxicity, and no drug has been found to treat or reduce cisplatin-induced cardiac side effects.
Does hesperidin prevent cisplatin-induced cardiotoxicity and oxidative stress in a rat model?
Does hesperidin prevent cisplatin-induced cardiotoxicity and oxidative stress in a rat model?
Hesperidin mitigates cisplatin-induced cardiotoxicity in a dose-dependent manner by preserving antioxidant capacity and maintaining autophagy pathways.
Hesperidin mitigated cisplatin cardiotoxicity in rats; hypothesis-generating, human trials needed before any clinical consideration.
Objective: Cisplatin is a well-known anticancer drug whose use has been limited due to a variety of side effects. Evidence has confirmed that cisplatin consumption is associated with cardiac toxicity. Unfortunately, no drug has yet been found to treat cardiac toxicity or reduce the side effects caused by cisplatin. However, hesperidin has been identified as an antioxidant agent which has protective effects on the heart tissue. This study explored the impact of hesperidin on cisplatin-induced cardiac toxicity through its antioxidant effect and adjustment of autophagy. Materials and Methods: day. A mixture of ketamine and xylazine was used to anesthetize all animals on day 8 to obtain blood and tissue samples and to record ECG. Results: The findings indicated that cisplatin led to an increase in creatine kinase-MB, lactate dehydrogenase, and malondialdehyde levels, and a reduction in total antioxidant capacity in heart tissue. Moreover, it reduced the expression of microtubule-associated protein light chain (LC3-II) and beclin-1. ECG parameters included: Heart rate (HR) and QRS voltage complex which were reduced by cisplatin. However, hesperidin (100, and 200 mg/kg) reversed these changes. Conclusion: Hesperidin could protect cardiac tissue against cisplatin administration by exerting its antioxidant effect and regulating autophagy in a dose-dependent manner.
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Kahkesh et al. (2026) studied Cisplatin-induced cardiotoxicity (n=40). Hesperidin vs. Cisplatin alone was evaluated on Cardiac injury, oxidative stress, autophagy markers, and ECG parameters at day 8. Hesperidin at 100 and 200 mg/kg significantly mitigated cisplatin-induced cardiotoxicity in rats by restoring antioxidant capacity, improving ECG parameters, and regulating autophagy.
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