NNMT is involved in deoxynivalenol-induced hepatocyte toxicity via promoting ferroptosis

Toxicology, Journal Year: 2025, Volume and Issue: unknown, P. 154084 - 154084

Published: Feb. 1, 2025

Language: Английский

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18β-Glycyrrhetinic acid protects against deoxynivalenol-induced liver injury via modulating ferritinophagy and mitochondrial quality control

Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 471, P. 134319 - 134319

Published: April 21, 2024

Language: Английский

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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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Simultaneous detection of mycotoxins and pesticides in human urine samples: A 24-h diet intervention study comparing conventional and organic diets in Spain

Food and Chemical Toxicology, Journal Year: 2024, Volume and Issue: 188, P. 114650 - 114650

Published: April 9, 2024

Language: Английский

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Resveratrol alleviates Mono-2-ethylhexyl phthalate-induced mitophagy, ferroptosis, and immunological dysfunction in grass carp hepatocytes by regulating the Nrf2 pathway

Journal of Environmental Management, Journal Year: 2024, Volume and Issue: 371, P. 123235 - 123235

Published: Nov. 6, 2024

Language: Английский

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Beyond Mortality: Exploring the Influence of Plant Phenolics on Modulating Ferroptosis—A Systematic Review

Antioxidants, Journal Year: 2024, Volume and Issue: 13(3), P. 334 - 334

Published: March 10, 2024

Ferroptosis is a recently discovered type of programmed cell death that mechanistically different from other types such as apoptosis, necroptosis, and autophagy. It characterized by the accumulation intracellular iron, overproduction reactive oxygen species, depletion glutathione, extensive lipid peroxidation lipids in membrane. was ferroptosis interconnected with many diseases, neurodegenerative ischemia/reperfusion injury, cancer, chronic kidney disease. Polyphenols, plant secondary metabolites known for bioactivities, are being extensively researched context their influence on which resulted great number publications showing need systematic review. In this review, an literature search performed. Databases (Scopus, Web Science, PubMed, ScienceDirect, Springer) were searched time span 2017 to November 2023, using keyword “ferroptosis” alone combination “flavonoid”, “phenolic acid”, “stilbene”, “coumarin”, “anthraquinone”, “chalcone”; after selection studies, we had 311 papers 143 phenolic compounds. total, 53 compounds showed ability induce ferroptosis, 110 able inhibit out those compounds, 20 both abilities depending model system. The most shikonin, curcumin, quercetin, resveratrol, baicalin. common modes action modulation Nrf2/GPX4 Nrf2/HO-1 axis iron metabolism.

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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Lithocholic Acid Alleviates Deoxynivalenol-Induced Inflammation and Oxidative Stress via PPARγ-Mediated Epigenetically Transcriptional Reprogramming in Porcine Intestinal Epithelial Cells

Journal of Agricultural and Food Chemistry, Journal Year: 2024, Volume and Issue: 72(10), P. 5452 - 5462

Published: March 1, 2024

Deoxynivalenol (DON) is a common mycotoxin that induces intestinal inflammation and oxidative damage in humans animals. Given lithocholic acid (LCA) has been suggested to inhibit inflammation, we aimed investigate the protective effects of LCA on DON-exposed porcine epithelial IPI-2I cells underlying mechanisms. Indeed, rescued DON-induced cell death reduced DON-stimulated inflammatory cytokine levels stress. Importantly, nuclear receptor PPARγ was identified as key transcriptional factor involved stress processes cells. The function found compromised, likely due hyperphosphorylation p38 ERK signaling pathways. In contrast, responses were restrained by via PPARγ-mediated reprogramming core antioxidant genes. Notably, PPARγ-modulated regulations could be attributed altered recruitments coactivator SRC-1/3 corepressor NCOR1/2, along with modified histone marks H3K27ac H3K18la. This study emphasizes actions epigenetically reprogramming, including acetylation lactylation.

Language: Английский

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Resveratrol Reorganizes the Impaired Cellular Functions of ARPE-19 Cells Created in Diabetes Model

Online Türk Sağlık Bilimleri Dergisi, Journal Year: 2025, Volume and Issue: 10(1), P. 38 - 44

Published: March 10, 2025

Objective: It is well known that high blood glucose levels can damage many visual functions. So, the study aimed to investigate effects of resveratrol on cellular lipid peroxidation (MDA), cytokines, VEGF-A and apoptosis in vitro diabetes model-induced ARPE-19 cells. Materials Methods: Six experimental groups were conceptualized as follows. 1-Control group: Received no treatment (Standard Growth Medium), 2-Mannitol Group (M): Cells incubated 19.5 mM Mannitol supplemented medium, 3-High Glucose (HG): (25 Glucose), 4-Resveratrol (R): with 100 µM Standard Medium, 5-Mannitol + Resveratrol (M+R), 6-High (HG+R). In All groups, cells for 48 hrs, MDA, IL-1β, TNF-α, Apoptosis measured. Results: High medium increased TNF-α while caused a significant decrement As result, prevented against related impaired conditions. Conclusions: conclusion, reverse disrupted functions by reducing oxidative stress supporting viability.

Language: Английский

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SIRT6 mitigates doxorubicin-induced cardiomyopathy via amelioration of mitochondrial dysfunction: A mechanistic study implicating the activation of the Nrf-2/FUNDC1 signaling axis

International Journal of Medical Sciences, Journal Year: 2025, Volume and Issue: 22(7), P. 1640 - 1657

Published: Feb. 28, 2025

Doxorubicin-induced myocardial injury, characterized by hypertrophy and heart failure (HF), represents a primary contributor to end-stage cardiovascular mortality associated with anthracycline drugs. Prior research has elucidated that SIRT6-mediated oxidative processes mitochondrial metabolic reprogramming are pivotal in sustaining energy metabolism during damage cardiomyocytes. In the aftermath of doxorubicin-induced fibrosis exacerbate impairment cardiac ejection function, resulting elevated oxygen consumption. This condition is accompanied disrupted ATP production, diminished biogenesis, inadequate synthesis new DNA, collectively triggering necroptosis apoptosis pathways. Our preliminary experimental results have confirmed SIRT6, traditional medicine, exerts cardioprotective effects. Nevertheless, interaction between SIRT6 Nrf-2-mediated biogenesis context HF remains inadequately understood. The generation mitochondria key mechanism involved DNA repair cell cycle management.

Language: Английский

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