18beta-glycyrrhetinic acid alleviates deoxynivalenol-induced hepatotoxicity by inhibiting GPX4-dependent ferroptosis

Toxicon, Journal Year: 2025, Volume and Issue: unknown, P. 108228 - 108228

Published: Jan. 1, 2025

Language: Английский

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Nuclear receptor coactive 4-mediated ferritinophagy: a key role of heavy metals toxicity

Archives of Toxicology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 10, 2025

Language: Английский

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Hesperidin Alleviates Hepatic Injury Caused by Deoxynivalenol Exposure through Activation of mTOR and AKT/GSK3β/TFEB Pathways

Journal of Agricultural and Food Chemistry, Journal Year: 2024, Volume and Issue: 72(25), P. 14349 - 14363

Published: June 13, 2024

Deoxynivalenol (DON) is a common agricultural mycotoxin that chemically stable and not easily removed from cereal foods. When organisms consume food made contaminated crops, it can be hazardous to their health. Numerous studies in recent years have found hesperidin (HDN) has hepatoprotective effects on wide range of toxins. However, few scholars explored the potential HDN attenuating DON-induced liver injury. In this study, we established low-dose DON exposure model intervened with three doses HDN, acting male C57 BL/6 mice AML12 cells, which served as vivo vitro models, respectively, investigate protective mechanism against exposure-induced The results suggested disrupted hepatic autophagic fluxes, thereby impairing structure function, significantly attenuated these changes. Further revealed alleviated excessive autophagy through mTOR pathway lysosomal dysfunction AKT/GSK3β/TFEB pathway. Overall, our study could ameliorate flux disorders via pathway, reducing

Language: Английский

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Zearalenone induces liver injury in mice through ferroptosis pathway

The Science of The Total Environment, Journal Year: 2024, Volume and Issue: 952, P. 175875 - 175875

Published: Aug. 30, 2024

Language: Английский

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Naringenin alleviates liver fibrosis by triggering autophagy-dependent ferroptosis in hepatic stellate cells

Heliyon, Journal Year: 2024, Volume and Issue: 10(7), P. e28865 - e28865

Published: March 29, 2024

Inhibition of activated hepatic stellate cells (HSCs) is a promising approach for treating liver fibrosis, and the ferroptosis has emerged as pivotal mechanism to achieve this inhibition. The effects naringenin, flavonoid with anti-inflammatory properties, have not been thoroughly examined in fibrosis. Therefore, we used cholestasis model study effect naringenin on Our findings demonstrated significant exacerbation tissue damage fibrosis mice subjected bile duct ligation (BDL), accompanied by substantial upregulation fibrogenesis-related gene expression. Notably, administration markedly alleviated injury these mice. Furthermore, exhibited inhibitory activation HSCs, concurrently inducing ferroptosis. Importantly, significantly increased autophagic activity HSCs. This was counteracted co-administration autophagy inhibitor 3-MA, leading notable reduction naringenin-induced HSC In BDL mice, mitigating suggesting potential correlation These results provide novel insights into molecular mechanisms highlight autophagy-dependent therapeutic strategy

Language: Английский

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Cu2O nanoparticles with morphology-dependent peroxidase mimic activity: a novel colorimetric biosensor for deoxynivalenol detection

Microchimica Acta, Journal Year: 2024, Volume and Issue: 191(10)

Published: Sept. 10, 2024

Language: Английский

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Targeting Ferroptosis and Ferritinophagy Improves Tooth Extraction Socket Healing in Type 2 Diabetes Mellitus Via Human Bone Marrow Mesenchymal Stem Cells Modulation

Published: Jan. 1, 2025

Language: Английский

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Ferritinophagy: multifaceted roles and potential therapeutic strategies in liver diseases

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: Feb. 25, 2025

Ferritinophagy, the selective autophagic degradation of ferritin to release iron, is emerging as a critical regulator iron homeostasis and key player in pathogenesis various liver diseases. This review comprehensively examines mechanisms, regulation, multifaceted roles ferritinophagy health disease. Ferritinophagy intricately regulated by several factors, including Nuclear Receptor Coactivator 4 (NCOA4), Iron regulatory proteins signaling pathways such mTOR AMPK. These mechanisms ensure proper utilization prevent overload, which can induce oxidative stress ferroptosis. In diseases, exhibits dual roles. fibrosis, promoting hepatic stellate cells (HSCs) cell senescence reduce fibrosis progression. However, non-alcoholic fatty disease (NAFLD), chronic may exacerbate injury through overload stress. hepatocellular carcinoma (HCC), be harnessed novel therapeutic strategy inducing ferroptosis cancer cells. Additionally, implicated drug-induced sepsis-associated damage, highlighting its broad impact on pathology. also explores crosstalk between other autophagy pathways, mitophagy lipophagy, collectively influence cellular Understanding these interactions essential for developing comprehensive strategies targeting multiple pathways. summary, complex dynamic process with significant implications provides an in-depth analysis ferritinophagy's potential target, emphasizing need further research elucidate role

Language: Английский

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Disorders of Iron Metabolism: A “Sharp Edge” of Deoxynivalenol-Induced Hepatotoxicity

Metabolites, Journal Year: 2025, Volume and Issue: 15(3), P. 165 - 165

Published: March 1, 2025

Background/Objectives: Deoxynivalenol (DON), known as vomitoxin, is one of the most common mycotoxins produced by Fusarium graminearum, with high detection rates in feed worldwide. Ferroptosis a novel mode cell death characterized lipid peroxidation and accumulation reactive oxygen species. Although it has been demonstrated that DON can induce ferroptosis liver, specific mechanisms pathways are still unknown. The aim this experiment was to investigate iron metabolism disorders livers mice, thereby triggering causing toxic damage liver. Methods: Male C57 mice were treated at 5 mg/kg BW concentration an vivo model. After sampling, organ coefficient monitoring, liver function test, histopathological analysis, Fe2+ content oxidative stress-related indexes performed. mRNA protein expression Nrf2 its downstream genes also detected using series methods including quantitative real-time PCR, immunofluorescence double-labeling, Western blotting analysis. Results: cause mouse. Specifically, we found mouse group exhibited pathological necrosis, inflammatory infiltration, cytoplasmic vacuolization, elevated relative weight, significant changes indexes. Meanwhile, substantial reduction levels glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), total antioxidant capacity (T-AOC) indicated caused stress Notably, exposure increased Malondialdehyde (MDA) which provides strong evidence for occurrence disorders. Most importantly, Nrf2, important pathway ferroptosis, along genes, heme oxygenase (HO-1), quinone oxidoreductase (NQO1), peroxidase (GPX4), solute carrier gene (SLC7a11), significantly inhibited group. Conclusions: Based on our results, closely associated DON-induced livers, suggesting maintaining hepatic homeostasis activating may be potential target mitigating hepatotoxicity future.

Language: Английский

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CYP2E1 mediated deoxynivalenol-induced hepatocyte toxicity by regulating ferroptosis

Toxicology, Journal Year: 2024, Volume and Issue: 508, P. 153923 - 153923

Published: Aug. 13, 2024

Language: Английский

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