Mechanisms of ferroptosis in Echinococcus granulosus cyst fluid-induced hepatic injury and the protective role of Nrf2 activation.
4 affiliations
- 1School of Basic Medicine, Chengdu Medical College, Sichuan, Chengdu, 610500, China.
- 2Department of Clinical Laboratory, WCSUH-Tianfu·Sichuan Provincial Children's Hospital, Meishan, 620020, China.
- 3Section for HepatoPancreatoBiliary Surgery, Department of General Surgery, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University & The Second Affiliated Hospital of Cheng-du, Chongqing Medical University, Chengdu, 610031, China. [email protected].
- 4School of Basic Medicine, Chengdu Medical College, Sichuan, Chengdu, 610500, China. [email protected].
Abstract
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.
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BibTeX
@article{chen2026mechanisms,
title = {{Mechanisms of ferroptosis in Echinococcus granulosus cyst fluid-induced hepatic injury and the protective role of Nrf2 activation.}},
author = {Jiaqi Chen and Jiangtao Cao and Jiuming Yan and Haiwen Li and Xinyi Du and Cheng Xiao Ke and Hailong Lv and Yufeng Jiang},
journal = {Parasitology research},
year = {2026},
month = aug,
doi = {10.1007/s00436-026-08719-w},
url = {https://europepmc.org/article/MED/42957908},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Mechanisms of ferroptosis in Echinococcus granulosus cyst fluid-induced hepatic injury and the protective role of Nrf2 activation.
AU - Jiaqi Chen
AU - Jiangtao Cao
AU - Jiuming Yan
AU - Haiwen Li
AU - Xinyi Du
AU - Cheng Xiao Ke
AU - Hailong Lv
AU - Yufeng Jiang
PY - 2026
DA - 2026/08/04
JO - Parasitology research
DO - 10.1007/s00436-026-08719-w
UR - https://europepmc.org/article/MED/42957908
AB - 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.
SN - 0932-0113
SN - 1432-1955
ER -