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

被引:14
作者
Qi, Yajun [1 ,2 ]
Fu, Shuang [3 ,4 ]
Pei, Donggen [5 ]
Fang, Qilu [1 ,2 ]
Xin, Wenxiu [1 ,2 ]
Yuan, Xiaohong [3 ,4 ]
Cao, Yingying [1 ,2 ]
Shu, Qi [1 ,2 ]
Mi, Xiufang [1 ,2 ]
Luo, Fang [1 ,2 ]
机构
[1] Univ Chinese Acad Sci, Zhejiang Canc Hosp, Canc Hosp, Dept Pharm, 38 Guangji Rd, Hangzhou 310022, Zhejiang, Peoples R China
[2] Chinese Acad Sci, Inst Canc & Basic Med IBMC, Dept Pharm, Hangzhou, Zhejiang, Peoples R China
[3] Univ Chinese Acad Sci, Zhejiang Canc Hosp, Canc Hosp, Dept Anesthesiol, Hangzhou, Zhejiang, Peoples R China
[4] Chinese Acad Sci, Inst Canc & Basic Med IBMC, Dept Anesthesiol, Hangzhou, Zhejiang, Peoples R China
[5] Nanjing Med Univ, Childrens Hosp, Dept Pharm, Nanjing, Peoples R China
关键词
Luteolin; cisplatin; oxidative stress; Keap1; Nrf2; INDUCED CARDIOTOXICITY; NRF2; PROGRESSION; MECHANISMS; INJURY; AMPK;
D O I
10.1080/10715762.2022.2067042
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:209 / 221
页数:13
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