阿霉素
肝损伤
GPX4
转铁蛋白
化学
铁蛋白
细胞保护
氧化应激
转铁蛋白受体
体内
炎症
药理学
谷胱甘肽过氧化物酶
生物化学
内科学
医学
超氧化物歧化酶
免疫学
生物
化疗
生物技术
作者
Bowen Yin,Jingyi Ren,Xuanyi Liu,Miaomiao Lu,Dan Huang,Yadong Zhang,Jinshi Zuo,Wen Rui,Huanting Pei,Siqi Zhu,Zhenao Zhang,Ziyi Wang,Yuxia Ma
标识
DOI:10.1016/j.jff.2024.106437
摘要
Hepatotoxicity is an significant side effect of doxorubicin (DOX), while astaxanthin (ASX) has the anti-liver injury biological functions. In this study, we utilized in vivo and in vitro methods to investigate the protective effect of ASX against DOX-induced hepatotoxicity and elucidate its potential mechanism. Our researchers measured liver injury indicators and the expression of ferroptosis-related protein (transferrin receptor 1 (TFRC), ferroportin 1 (FPN1), ferritin light chain (FTL), ferritin heavy chain-1 (FTH1), glutathione peroxidase 4 (GPX4), and solute carrier family 7 member 11 (SLC7A11)) in rats and HepG2 cells. We found that ASX could effectively reduce ferroptosis level and relieve a range of DOX-caused manifestations of liver injury, including inflammation and oxidative damage. ASX may play the same role as ferroptosis inhibitor, Fer-1 and DFP, in this process. The findings demonstrated that the intervention with ASX ameliorated the DOX-induced liver injury by mitigating the DOX-induced ferroptosis through inhibiting iron accumulation.
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