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<p>Cystic echinococcosis (CE) is a globally distributed parasitic zoonosis caused by infection with <i>Echinococcus granulosus.</i> This study investigated the ferroptosis mechanism in hepatocyte injury induced by <i>Echinococcus granulosus</i> cyst fluid (EgCF) and its relationship with the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway using an in vitro model. We employed the Cell Counting Kit-8(CCK-8) assay, Calcein AM/PI staining, and flow cytometry to assess cell viability, reactive oxygen species (ROS) production, and mitochondrial membrane potential (MMP). Additionally, we measured lipid peroxides, malondialdehyde (MDA), glutathione (GSH), and ferrous iron (Fe²⁺) levels. Western blot analysis examined the expression of glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11(SLC7A11), prostaglandin-endoperoxide synthase 2 (Ptgs2), ferritin heavy chain (FTH1), Nrf2, and heme oxygenase-1 (HO-1). Results indicated that EgCF inhibited hepatocyte proliferation and promoted hepatocyte apoptosis while inducing ferroptosis. Treatment with ferroptosis inhibitors Deferoxamine (DFO) or N-acetylcysteine (NAC) significantly attenuated EgCF-induced cytotoxicity. Nrf2 activation markedly mitigated EgCF-induced hepatocyte injury. This study elucidates the role of EgCF-induced ferroptosis and Nrf2 signaling in CE-associated liver injury, providing novel theoretical insights and new targets for disease prevention and treatment strategies.</p>

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Mechanisms of ferroptosis in Echinococcus granulosus cyst fluid-induced hepatic injury and the protective role of Nrf2 activation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月4日

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  • Jiaqi Chen,
  • Jiangtao Cao,
  • Jiuming Yan,
  • Haiwen Li,
  • Xinyi Du,
  • Cheng xiao Ke,
  • Hailong Lv,
  • Yufeng Jiang

摘要

Cystic echinococcosis (CE) is a globally distributed parasitic zoonosis caused by infection with Echinococcus granulosus. This study investigated the ferroptosis mechanism in hepatocyte injury induced by Echinococcus granulosus cyst fluid (EgCF) and its relationship with the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway using an in vitro model. We employed the Cell Counting Kit-8(CCK-8) assay, Calcein AM/PI staining, and flow cytometry to assess cell viability, reactive oxygen species (ROS) production, and mitochondrial membrane potential (MMP). Additionally, we measured lipid peroxides, malondialdehyde (MDA), glutathione (GSH), and ferrous iron (Fe²⁺) levels. Western blot analysis examined the expression of glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11(SLC7A11), prostaglandin-endoperoxide synthase 2 (Ptgs2), ferritin heavy chain (FTH1), Nrf2, and heme oxygenase-1 (HO-1). Results indicated that EgCF inhibited hepatocyte proliferation and promoted hepatocyte apoptosis while inducing ferroptosis. Treatment with ferroptosis inhibitors Deferoxamine (DFO) or N-acetylcysteine (NAC) significantly attenuated EgCF-induced cytotoxicity. Nrf2 activation markedly mitigated EgCF-induced hepatocyte injury. This study elucidates the role of EgCF-induced ferroptosis and Nrf2 signaling in CE-associated liver injury, providing novel theoretical insights and new targets for disease prevention and treatment strategies.