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Critical Role of Pyroptosis in Deoxynivalenol-Induced Renal Tubular Epithelial Damage in Mice
Yuetong Wang1, Xiaohui Liu1, Hao Chen1
1College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Abstract:
Deoxynivalenol (DON) is widely distributed and chemically stable, posing a serious health risk. The kidney, as the primary metabolic organ, is a major target of DON toxicity, yet its mechanism remains unresolved. Using C57BL/6 mice and TCMK-1 cells, we established DON-induced injury models and observed activation of the NOD-like receptor protein 3 (NLRP3) inflammasome, Caspase-1 activation, and cleavage of gasdermin D (GSDMD) to its N-terminal fragment (GSDMD-N). GSDMD-N translocated to the plasma membrane, formed pores, and promoted release of inflammatory mediators, culminating in pyroptosis. Treatment with the antioxidant N-acetyl-l-cysteine (NAC) significantly reduced intracellular reactive oxygen species (ROS) and suppressed pyroptosis-associated markers (P < 0.05), implicating oxidative stress as a key upstream driver. Collectively, these data indicate that DON induces renal tubular epithelial cell injury via the ROS/NLRP3/GSDMD-N pathway.
Insights
Deoxynivalenol (DON) causes kidney damage by triggering programmed cell death called pyroptosis. This occurs through the ROS/NLRP3/GSDMD-N pathway, but antioxidants like NAC can reduce this toxicity.
Area of Science:
- Toxicology
- Cell Biology
- Immunology
Background:
- Deoxynivalenol (DON) is a widespread mycotoxin posing significant health risks.
- The kidney is a primary target for DON toxicity, but the underlying mechanisms are not fully understood.
Purpose of the Study:
- To elucidate the mechanism of DON-induced kidney injury.
- To investigate the role of the NLRP3 inflammasome and pyroptosis in DON toxicity.
Main Methods:
- Established DON-induced injury models in C57BL/6 mice and TCMK-1 cells.
- Analyzed the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome, Caspase-1, and gasdermin D (GSDMD).
- Assessed the impact of N-acetyl-l-cysteine (NAC) on reactive oxygen species (ROS) and pyroptosis markers.
Main Results:
- DON exposure activated the NLRP3 inflammasome, Caspase-1, and induced GSDMD cleavage.
- GSDMD-N formation and translocation led to pyroptosis and inflammatory mediator release.
- NAC treatment reduced ROS levels and suppressed pyroptosis, indicating oxidative stress involvement.
Conclusions:
- DON induces renal tubular epithelial cell injury through the ROS/NLRP3/GSDMD-N pathway.
- Oxidative stress is a critical upstream factor in DON-induced pyroptosis.
- Targeting oxidative stress may offer a therapeutic strategy against DON nephrotoxicity.
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