Key result
Luteolin attenuated cisplatin-induced cardiac dysfunction and oxidative stress in vivo and in HL-1 cells by modulating the Keap1/Nrf2 signaling pathway.
Why the study?
Cisplatin-induced cardiotoxicity limits its clinical application, and the effect of luteolin on cisplatin-induced cardiac damage remains unclear.
Lut may attenuate cisplatin cardiotoxicity via Keap1/Nrf2 in preclinical models; leaves open clinical translation and human efficacy.
Cardiovascular complications are a well-documented limitation of cancer chemotherapy. Cisplatin-induced cardiotoxicity threatens the health and life of patients, and limits the application of cisplatin. Oxidative stress is the main mechanism underlying cisplatin-induced cardiac toxicity. Luteolin (Lut) has been reported to possess cardioprotective properties by activating nuclear factor-E2-related factor 2 (Nrf2) -mediated antioxidant response. However, the effect of Lut on cisplatin-induced cardiac damage remains unclear. In this study, we revealed that Lut exerted a protective effect against cisplatin-induced cardiac dysfunction and injury in vivo. In HL-1 cells, Lut was observed to dramatically reduce cisplatin-induced apoptosis and oxidative stress by modulating the Kelch-like epichlorohydrin-associated protein 1 (Keap1)/Nrf2 pathway. Altogether, these findings suggested that Lut showed promise in attenuating cisplatin-induced cardiac injury and might be considered a protective drug candidate for chemotherapy-associated cardiovascular complications.
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Qi et al. (2022) studied Cisplatin-induced cardiotoxicity. Luteolin was evaluated on Cisplatin-induced cardiac dysfunction, apoptosis, and oxidative stress. Luteolin attenuated cisplatin-induced cardiac dysfunction and oxidative stress in vivo and in HL-1 cells by modulating the Keap1/Nrf2 signaling pathway.
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