肝细胞
对乙酰氨基酚
氧化应激
化学
肝损伤
活性氧
活力测定
细胞凋亡
程序性细胞死亡
药理学
信号转导
脂质过氧化
细胞生物学
生物化学
生物
体外
作者
Huiyi Li,Qiqing Weng,Shuai Gong,Wei‐xian Zhang,Jiaqi Wang,Yuqiao Huang,Yuanjun Li,Jiao Guo,Tian Lan
出处
期刊:Food & Function
[Royal Society of Chemistry]
日期:2023-01-01
卷期号:14 (4): 1884-1896
被引量:97
摘要
. Cell viability was assayed by the CCK8 assay. Mitochondrial reactive oxygen species (ROS) in L02 cells were detected by MitoSox fluorescence. KA reversed the APAP-induced decrease in cell viability and GSH levels and inhibited the accumulation of intracellular ROS. Furthermore, KA activated the Nrf2 pathway and upregulated Gpx4 in mouse livers and L02 cells to inhibit ferroptosis induced by APAP. Finally, molecular docking indicated the potential interaction of KA with Keap1. Taken together, KA ameliorated oxidative stress and ferroptosis-mediated AILI by activating Nrf2 signaling.
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