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<p>Ferroptosis is an iron-dependent form of regulated cell death characterized by excessive lipid peroxidation and has been implicated in the pathogenesis of hepatic injury. However, whether quercetin (Que) protects against iron overload-induced liver injury and the underlying mechanisms remain unclear. In this study, we established a mouse model of iron overload by intraperitoneal injection of iron dextran and, in parallel, treated Hep G2 cells with Ferric citrate (FAC) to mimic iron overload in vitro. The protective effects of Que on liver injury were evaluated through histopathological examination, biochemical assays, Western blotting, and RT-qPCR in vivo, while cell viability, ROS levels, and ferroptosis-related markers were assessed in vitro. Iron overload markedly impaired liver function, increased ROS accumulation, and disrupted the expression of iron metabolism- and ferroptosis-related markers in both in vivo and in vitro. Que significantly alleviated these alterations, reduced oxidative stress, and improved iron metabolism-related changes in both models. These protective effects were accompanied by modulation of the NRF2/GPX4 signaling pathway. Collectively, our findings suggest that Que attenuates iron overload-induced liver injury and ferroptosis, potentially through regulation of the NRF2/GPX4 pathway, as corroborated by complementary in vivo and in vitro evidence.</p>

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Quercetin ameliorates iron overload-induced liver injury via NRF2/GPX4 pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月1日

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  • Zhibin Sun,
  • Zhihong Kong,
  • Xiaoyi Wang,
  • Wenzheng Yuan,
  • Liuyang Zhou,
  • Zixuan Yang,
  • Chen Guo,
  • Lanqiong Yan,
  • Huigen Feng,
  • Huanhuan Hu,
  • Guojie Ji

摘要

Ferroptosis is an iron-dependent form of regulated cell death characterized by excessive lipid peroxidation and has been implicated in the pathogenesis of hepatic injury. However, whether quercetin (Que) protects against iron overload-induced liver injury and the underlying mechanisms remain unclear. In this study, we established a mouse model of iron overload by intraperitoneal injection of iron dextran and, in parallel, treated Hep G2 cells with Ferric citrate (FAC) to mimic iron overload in vitro. The protective effects of Que on liver injury were evaluated through histopathological examination, biochemical assays, Western blotting, and RT-qPCR in vivo, while cell viability, ROS levels, and ferroptosis-related markers were assessed in vitro. Iron overload markedly impaired liver function, increased ROS accumulation, and disrupted the expression of iron metabolism- and ferroptosis-related markers in both in vivo and in vitro. Que significantly alleviated these alterations, reduced oxidative stress, and improved iron metabolism-related changes in both models. These protective effects were accompanied by modulation of the NRF2/GPX4 signaling pathway. Collectively, our findings suggest that Que attenuates iron overload-induced liver injury and ferroptosis, potentially through regulation of the NRF2/GPX4 pathway, as corroborated by complementary in vivo and in vitro evidence.