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<p>Cystic echinococcosis (CE), which primarily affects the liver, is associated with hepatocyte injury, although the underlying cellular and molecular mechanisms remain unclear. The aim of this study was to determine whether hepatocyte injury caused by <i>Echinococcus granulosus</i> sensu lato involves pyroptosis mediated through the ROS-NLRP3 inflammasome pathway. AML-12 hepatocytes were exposed to <i>E. granulosus</i> excretory-secretory products (ESPs), and cell viability, LDH release, cell death, and NLRP3 inflammasome-mediated pyroptosis were evaluated. The results indicated that ESP treatment reduced cell viability, increased LDH release and cell death, and upregulated markers of NLRP3 inflammasome-dependent pyroptosis. Pharmacological inhibition of NLRP3 with MCC950 markedly attenuated ESP-induced cytotoxicity and pyroptosis, confirming the critical role of NLRP3 activation in this process. Additionally, the ROS scavenger <i>N</i>-acetyl-<span>L</span>-cysteine (NAC) suppressed pyroptosis and reduced inflammasome activation, indicating that ESP-induced pyroptosis is ROS dependent. All of these results point to the possibility that ESPs cause hepatocyte damage in CE by inducing hepatocyte pyroptosis via the ROS-NLRP3 inflammasome pathway.</p>

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ROS-NLRP3 participates in the pyroptosis response of excretory-secretory products from protoscoleces of Echinococcus granulosus in hepatocytes

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月20日

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  • Jiangtao Cao,
  • Jiaqi Chen,
  • Haiwen Li,
  • Hailong Lv,
  • Yufeng Jiang

摘要

Cystic echinococcosis (CE), which primarily affects the liver, is associated with hepatocyte injury, although the underlying cellular and molecular mechanisms remain unclear. The aim of this study was to determine whether hepatocyte injury caused by Echinococcus granulosus sensu lato involves pyroptosis mediated through the ROS-NLRP3 inflammasome pathway. AML-12 hepatocytes were exposed to E. granulosus excretory-secretory products (ESPs), and cell viability, LDH release, cell death, and NLRP3 inflammasome-mediated pyroptosis were evaluated. The results indicated that ESP treatment reduced cell viability, increased LDH release and cell death, and upregulated markers of NLRP3 inflammasome-dependent pyroptosis. Pharmacological inhibition of NLRP3 with MCC950 markedly attenuated ESP-induced cytotoxicity and pyroptosis, confirming the critical role of NLRP3 activation in this process. Additionally, the ROS scavenger N-acetyl-L-cysteine (NAC) suppressed pyroptosis and reduced inflammasome activation, indicating that ESP-induced pyroptosis is ROS dependent. All of these results point to the possibility that ESPs cause hepatocyte damage in CE by inducing hepatocyte pyroptosis via the ROS-NLRP3 inflammasome pathway.