Key result
Quercetin pretreatment mitigates cisplatin-induced cardiomyocyte toxicity and oxidative stress via Nrf2/HO-1 signaling.
Why the study?
Cisplatin causes cardiotoxicity that limits its clinical use, and whether quercetin can protect against cisplatin-induced apoptosis and cellular damage in cardiomyocytes is unclear.
Does quercetin pretreatment prevent cisplatin-induced oxidative damage and apoptosis in H9c2 cardiomyocytes?
Population
H9c2 cardiomyocytes treated with cisplatin (40 μM)
Comparison
Cisplatin with vs without quercetin pretreatment
Design
In vitro controlled laboratory study
Follow-up
24 h
Authors
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Quercetin may protect against cisplatin cardiotoxicity in vitro; hypothesis-generating and requires in vivo and clinical validation before any practice consideration.
Does quercetin pretreatment prevent cisplatin-induced oxidative damage and apoptosis in H9c2 cardiomyocytes?
Quercetin demonstrates potential as a protective agent against cisplatin-induced cardiotoxicity through antioxidant and anti-inflammatory mechanisms in a preclinical cardiomyocyte model.
Wang et al. (2022) studied Cisplatin-induced cardiotoxicity. Quercetin vs. Cisplatin alone was evaluated on Cytotoxicity, apoptosis, and oxidative stress. Quercetin pretreatment mitigated cisplatin-induced cytotoxicity, apoptosis, and oxidative stress in H9c2 cardiomyocytes via the Nrf2/HO-1 signaling pathway.
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