Hormetic Nutrition and Redox Regulation in Gut–Brain Axis Disorders

Antioxidants, Journal Year: 2024, Volume and Issue: 13(4), P. 484 - 484

Published: April 18, 2024

The antioxidant and anti-inflammatory effects of hormetic nutrition for enhancing stress resilience overall human health have received much attention. Recently, the gut-brain axis has attracted prominent interest preventing therapeutically impacting neuropathologies gastrointestinal diseases. Polyphenols polyphenol-combined nanoparticles in synergy with probiotics shown to improve gut bioavailability blood-brain barrier (BBB) permeability, thus inhibiting oxidative stress, metabolic dysfunction inflammation linked dysbiosis ultimately onset progression central nervous system (CNS) disorders. In accordance hormesis, polyphenols display biphasic dose-response by activating at a low dose Nrf2 pathway resulting upregulation

Language: Английский

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Melatonin protects against cadmium-induced endoplasmic reticulum stress and ferroptosis through activating Nrf2/HO-1 signaling pathway in mice lung

Food and Chemical Toxicology, Journal Year: 2025, Volume and Issue: unknown, P. 115324 - 115324

Published: Feb. 1, 2025

Language: Английский

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Ferritinophagy Is Critical for Deoxynivalenol-Induced Liver Injury in Mice

Journal of Agricultural and Food Chemistry, Journal Year: 2024, Volume and Issue: 72(12), P. 6660 - 6671

Published: March 19, 2024

Background: Deoxynivalenol (DON) contamination, pervasive throughout all stages of food production and processing, presents a significant threat to human health. The degradation ferritin mediated by nuclear receptor coactivator 4 (NCOA4), termed ferritinophagy, plays crucial role in maintaining iron homeostasis regulating ferroptosis. Aim: This study aims elucidate the ferritinophagy ferroptosis DON-induced liver injury. Methods: Male mice AML12 cells were subjected varying doses DON, serving as vivo vitro models, respectively. Protein expression was assessed using immunofluorescence western blot techniques. Co-immunoprecipitation employed investigate protein–protein interactions. Results: Our findings demonstrate that DON triggers hepatocyte ferritinophagy-dependent manner. Specifically, impedes activation mammalian target rapamycin complex 1 (mTORC1) inhibiting RAC1's binding mTOR, thereby ultimately inducing autophagy. Concurrently, amplifies NCOA4's affinity for facilitating NCOA4 phosphorylation through ataxia-telangiectasia mutated kinase (ATM), thus promoting autophagy-dependent ferritin. Both autophagy inhibition suppression ameliorate Conclusion: concludes facilitates NCOA4-mediated via ATM–NCOA4 pathway, subsequently liver.

Language: Английский

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Neuropeptide substance P attenuates colitis by suppressing inflammation and ferroptosis via the cGAS-STING signaling pathway

International Journal of Biological Sciences, Journal Year: 2024, Volume and Issue: 20(7), P. 2507 - 2531

Published: Jan. 1, 2024

Neuropeptide substance P (SP) belongs to a family of bioactive peptides and regulates many human diseases. This study aims investigate the role underlying mechanisms SP in colitis. Here, activated SP-positive neurons increased expression were observed dextran sodium sulfate (DSS)-induced colitis lesions mice. Administration exogenous efficiently ameliorated clinical symptoms, impaired intestinal barrier function, inflammatory response. Mechanistically, protected mitochondria from damage caused by DSS or TNF-α exposure, preventing mitochondrial DNA (mtDNA) leakage into cytoplasm, thereby inhibiting cyclic GMP-AMP synthase-stimulator interferon genes (cGAS-STING) pathway. can also directly prevent STING phosphorylation through neurokinin-1 receptor (NK1R), activation TBK1-IRF3 signaling Further studies revealed that alleviated TNF-α-induced ferroptosis process, which was associated with repressing cGAS-STING Notably, we identified NK1R inhibition reversed effects on inflammation via Collectively, unveil attenuates suppressing mtDNA-cGAS-STING acting pathway, contributing improving an NK1R-dependent manner. These findings provide novel mechanism regulating ulcerative (UC) disease.

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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Orally administered metal–organic framework nanocubes for sequence-targeted quercetin delivery in colitis alleviation

Chemical Engineering Journal, Journal Year: 2025, Volume and Issue: unknown, P. 160373 - 160373

Published: Feb. 1, 2025

Language: Английский

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Naringin Suppresses CoCl2-Induced Ferroptosis in ARPE-19 Cells

Antioxidants, Journal Year: 2025, Volume and Issue: 14(2), P. 236 - 236

Published: Feb. 18, 2025

Hypoxic damage to retinal pigment epithelial (RPE) cells and subsequent neovascularization are key factors in the pathogenesis of branch vein occlusion (BRVO). Naringin (NG), a naturally occurring flavanone glycoside, has demonstrated significant antioxidant anti-neovascular activities. However, regulatory effects mechanisms NG on ferroptosis BRVO yet be explored. Our study aimed investigate protective RPE under hypoxic stress elucidate underlying molecular mechanisms. findings revealed that significantly reduced cytotoxicity induced by cobaltous chloride (CoCl2) also inhibited vascular proliferation retina, thereby attenuating choroidal neovascularization. pretreatment largely countered overproduction reactive oxygen species (ROS) malondialdehyde (MDA) triggered damage, while restoring levels antioxidants glutathione (GSH) superoxide dismutase (SOD). Furthermore, activated expression hypoxia-inducible factor-1 alpha (HIF-1α) its downstream heme oxygenase-1 (HO-1) NADPH dehydrogenase (NQO1). In conclusion, not only inhibits but alleviates inflammation modulating HO-1/GPX4 pathway inhibit ferroptosis. These highlight potential as promising therapeutic agent for treatment BRVO.

Language: Английский

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Quercetin alleviates LPS/iE-DAP-induced liver injury by suppressing ferroptosis via regulating ferritinophagy and intracellular iron efflux

Redox Biology, Journal Year: 2025, Volume and Issue: 81, P. 103557 - 103557

Published: Feb. 18, 2025

Ruminal dysbiosis-induced liver injury is prevalent in dairy cows, yet its underlying mechanisms remain incompletely understood. Ferroptosis, a newly identified form of programmed cell death distinct from apoptosis and necrosis, has been implicated various diseases by emerging studies. In the present study, lipopolysaccharide (LPS) γ-D-glutamyl-meso-diaminopimelic acid (iE-DAP) were employed to establish vitro vivo models using bovine hepatocytes mice, respectively. It was observed that noncytotoxic iE-DAP alone did not influence lipid peroxidation or GPX4, but exacerbated LPS-induced ferroptosis hepatocyte injury. Notably, co-treatment with LPS (LPS/iE-DAP)-induced mitigated intervention inhibitor ferrostatin-1 (Fer-1). Mechanistically, activated IL-6/STAT3 signaling pathway found mediate LPS/iE-DAP-induced ferroptosis. Suppression IL-6/STAT3, either through IL6 STAT3 knockdown pharmacological intervention, reduced Fe2+ accumulation alleviated ferroptotic death. Further investigations enhanced ferritinophagy impaired iron export. Either disrupting knocking down NCOA4 restoring export via HAMP relieved intracellular overload inhibited Specifically, LPS/iE-DAP treatment increased interaction between hepcidin ferroportin, promoting ferroportin ubiquitination degradation, thereby blocking efflux. Furthermore, we provided several evidence prove quercetin pretreatment decreasing hepatic targeting vivo, effects reversed addition recombinant IL-6. Based on these findings, concluded triggering regulating IL-6/STAT3/ferritinophagy-dependent release IL-6/STAT3/hepcidin/ferroportin-dependent export, while could alleviate this inhibiting pathway. This study provides novel insights into whereby ruminal dysbiosis induces presents prospective solution for

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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