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<p>Acute liver injury (ALI) is a global health issue associated with high mortality rates and has garnered significant clinical attention. Curcumin (CUR), a natural compound derived from turmeric rhizomes, possesses diverse therapeutic benefits. This article examines the mechanism by which CUR intervenes in ALI induced by carbon tetrachloride (CCl<sub>4</sub>). Hepatocellular carcinoma (HepG2) cell injury was induced with 5&#xa0;mM CCl<sub>4</sub>, and the effects of CUR (5, 10, and 20&#xa0;µM) were tested using various methods, including ferroptosis inducers and inhibitors, fluorescence staining, Western blot, RT-qPCR, and electron microscopy. CCl<sub>4</sub> treatment significantly increased lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), malondialdehyde (MDA), reactive oxygen species (ROS), and the expression of thioredoxin-interacting protein (TXNIP), NLRP3 inflammasome, and transferrin receptor 1 (TfR1). It also reduced total superoxide dismutase (T-SOD), glutathione (GSH), thioredoxin-1 (Trx-1), glutathione peroxidase 4 (GPX4), SLC7A11, and mitochondrial membrane potential, leading to mitochondrial damage. CUR effectively reversed these changes by inhibiting oxidative stress and ferroptosis through the TXNIP/NLRP3 pathway and the SLC7A11/GSH/GPX4 axis.</p> Graphical Abstract <p></p>

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Curcumin alleviates ferroptosis in CCl₄-induced acute liver injury in vitro: involvement of TXNIP/NLRP3 inhibition and SLC7A11/GSH/GPX4 activation

  • 期刊论文

  • 发表日期：

    2025年10月24日

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  • Wei Zhang,
  • Ziqi Liu,
  • Changle Dong,
  • Huimin Yang,
  • Yunchao Zhang,
  • Shuo Li,
  • Yinsheng Qiu,
  • Lingyun Xu

摘要

Acute liver injury (ALI) is a global health issue associated with high mortality rates and has garnered significant clinical attention. Curcumin (CUR), a natural compound derived from turmeric rhizomes, possesses diverse therapeutic benefits. This article examines the mechanism by which CUR intervenes in ALI induced by carbon tetrachloride (CCl4). Hepatocellular carcinoma (HepG2) cell injury was induced with 5 mM CCl4, and the effects of CUR (5, 10, and 20 µM) were tested using various methods, including ferroptosis inducers and inhibitors, fluorescence staining, Western blot, RT-qPCR, and electron microscopy. CCl4 treatment significantly increased lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), malondialdehyde (MDA), reactive oxygen species (ROS), and the expression of thioredoxin-interacting protein (TXNIP), NLRP3 inflammasome, and transferrin receptor 1 (TfR1). It also reduced total superoxide dismutase (T-SOD), glutathione (GSH), thioredoxin-1 (Trx-1), glutathione peroxidase 4 (GPX4), SLC7A11, and mitochondrial membrane potential, leading to mitochondrial damage. CUR effectively reversed these changes by inhibiting oxidative stress and ferroptosis through the TXNIP/NLRP3 pathway and the SLC7A11/GSH/GPX4 axis.

Graphical Abstract