黄素通过调节PERK/Nrf2/HO-1信号通路来诱导肝细胞癌中的铁亡
Cheng Yuan1,2, Ruiwen Liu1, Xinming Xu1
1Department of Hepatobiliary Surgery, Kunshan Hospital Affiliated to Jiangsu University, Suzhou, China.
Translational cancer research
|December 11, 2025
概括
黄素通过PERK/Nrf2/HO-1通路诱导铁亡,抑制肝细胞癌 (HCC) 细胞活力. 这种天然化合物显示出作为HCC治疗新型治疗剂的前景.
科学领域:
- 在瘤学瘤学.
- 生物化学 生物化学
- 分子生物学分子生物学
背景情况:
- 肝细胞癌 (HCC) 呈现出高恶性和微妙的早期症状,往往需要药物治疗而不是手术.
- 目前的HCC治疗方法是不理想的,这凸显了对新型治疗剂的需求.
- 黄素是一种天然化合物,表现出抗癌性质,并正在研究其抗HCC机制.
研究的目的:
- 为了阐明黄素的抗HCC机制.
- 研究黄素作为HCC治疗候选药物的潜力.
主要方法:
- 细胞计数工具-8 (CCK-8) 测试细胞活力.
- 生物化学工具包和光探针用于测量谷氨 (GSH),甲 (MDA),活性氧物种 (ROS) 和铁含量.
- 西部涂抹检测PERK,Nrf2,HO-1和GPX4.4的蛋白质表达.
主要成果:
- 黄素抑制了HCC细胞活力,这种效应被铁灭抑制剂 (Fer-1,DFO) 逆转.
- 黄素治疗增加了细胞内铁,Fe2+,MDA和ROS,同时降低了GSH水平.
- 库尔库降低了GPX4的调节,并提高了PERK,Nrf2和HO-1的调节,表明PERK/Nrf2/HO-1通路的激活.
结论:
- 黄素通过PERK/Nrf2/HO-1信号通路诱导HCC细胞中的铁亡.
- 这些发现表明黄素具有作为HCC的新型治疗剂的潜力.
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