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February 2, 2026ToxicsOpen Access

AHR-CYP1A1 Axis Perturbation and Necroptosis in 1,2-Dichloroethane Hepatotoxicity: Elucidation by an Integrated Network Toxicology and In Vitro Validation

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Authors

YLYichang LiuHLHuijie LuoZTZhiling Tian

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Overview

Integrated network toxicology reveals mechanisms of necroptosis in hepatotoxicity from 1,2-DCE, suggesting therapeutic targets.

Key Points

  • This research aims to elucidate the mechanisms of liver injury caused by 1,2-DCE, focusing on necroptosis and the AHR-CYP1A1 pathway.
  • Integrated network toxicology analysis and molecular docking were performed.
  • In vitro experiments used THLE-2 hepatocyte models to assess viability and necroptosis.
  • Cell viability was measured using CCK-8 assays.
  • Molecular mechanisms were analyzed through protein level assessments and phosphorylation status.
  • 1,2-DCE reduced hepatocyte viability in a concentration-dependent manner.
  • AHR translocated to the nucleus rapidly after exposure, and CYP1A1 expression was initially upregulated.
  • Intracellular ROS levels increased after 24 hours, indicating oxidative stress.
  • CYP1A1 expression was suppressed after 48 hours alongside markers of necroptosis.

Cite This Study

Liu et al. (2026) studied this question.

synapsesocial.com/papers/6980fe57c1c9540dea81055chttps://doi.org/10.3390/toxics14020136
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