Luteolin attenuated cisplatin-induced cardiac dysfunction and oxidative stress via modulation of Keap1/Nrf2 signaling pathway

• Published in: Free radical research Vol. 56; no. 2; pp. 209 - 221
• Main Authors: Qi, Yajun, Fu, Shuang, Pei, Donggen, Fang, Qilu, Xin, Wenxiu, Yuan, Xiaohong, Cao, Yingying, Shu, Qi, Mi, Xiufang, Luo, Fang
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 01.02.2022
• Subjects: Apoptosis; cisplatin; Cisplatin - adverse effects; Epichlorohydrin - pharmacology; Heart Diseases; Humans; Keap1; Kelch-Like ECH-Associated Protein 1 - metabolism; Luteolin; Luteolin - pharmacology; Luteolin - therapeutic use; NF-E2-Related Factor 2 - metabolism; Nrf2; Oxidative Stress; Signal Transduction; Keap1; Luteolin; cisplatin; Nrf2; oxidative stress
• ISSN: 1071-5762; 1029-2470
• DOI: 10.1080/10715762.2022.2067042

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.