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Quercetin alleviates high fluoride-induced hepatocyte ferroptosis via regulating the ROS/PERK signaling pathway
Chao Song1, Rui Yu1, Aiguo Zhang1
1College of Veterinary Medicine, Henan University of Animal Husbandry and Economy, Zhengzhou, Henan 450046, China.
Ecotoxicology and Environmental Safety
|July 23, 2026
Summary
Quercetin (Que) protects against fluoride-induced liver injury by inhibiting ferroptosis. It reduces oxidative stress and inflammation by targeting the ROS/PERK pathway, offering potential therapeutic benefits.
Area of Science:
- Biochemistry
- Toxicology
- Cell Biology
Background:
- Ferroptosis is linked to fluoride-induced liver damage.
- Quercetin (Que), a flavonoid, shows anti-ferroptotic properties.
Purpose of the Study:
- To investigate Que's protective effects against sodium fluoride (NaF)-induced ferroptosis.
- To elucidate the molecular mechanisms behind Que's hepatoprotective actions.
Main Methods:
- In vivo studies in NaF-exposed mice.
- In vitro assays using AML-12 cells.
- Molecular docking and dynamics simulations.
- Pharmacological intervention with PERK modulators.
Main Results:
- Que restored liver function, reduced hepatic lesions, and alleviated mitochondrial damage in NaF-treated mice.
- Que suppressed NaF-induced apoptosis and inflammation.
- Que inhibited reactive oxygen species (ROS), lipid peroxidation, and iron overload, while boosting glutathione levels.
- Que suppressed the ROS/PERK signaling pathway, confirmed by molecular docking and pharmacological interventions.
Conclusions:
- Quercetin mitigates NaF-induced hepatic ferroptosis by inhibiting the ROS/PERK signaling pathway.
- Que demonstrates potential as a therapeutic agent for high fluoride-induced hepatotoxicity.
