Neuroscience, Год журнала: 2024, Номер 554, С. 72 - 82
Опубликована: Июль 14, 2024
Язык: Английский
Advanced Healthcare Materials, Год журнала: 2024, Номер 13(11)
Опубликована: Янв. 19, 2024
Abstract Drug‐induced liver injury (DILI) is a severe condition characterized by impaired function and the excessive activation of ferroptosis. Unfortunately, there are limited options currently available for preventing or treating DILI. In this study, MnO 2 nanoflowers (MnO Nfs) with remarkable capabilities mimicking essential antioxidant enzymes, including catalase, superoxide dismutase (SOD), glutathione peroxidase successfully synthesized, SOD dominant enzyme among them density functional theory. Notably, Nfs demonstrate high efficiency in effectively eliminating diverse reactive oxygen species (ROS) such as hydrogen peroxide (H O ), anion (O •− hydroxyl radical (•OH). Through vitro experiments, it demonstrated that significantly enhance recovery intracellular content, acting potent inhibitor ferroptosis even presence activators. Moreover, exhibit excellent accumulation properties, providing robust protection against oxidative damage. Specifically, they attenuate acetaminophen‐induced inhibiting ferritinophagy activating P62‐NRF2‐GPX4 antioxidation signaling pathways. These findings highlight ROS scavenging ability hold great promise an innovative potential clinical therapy DILI other ROS‐related diseases.
Язык: Английский
Процитировано
16
Signal Transduction and Targeted Therapy, Год журнала: 2025, Номер 10(1)
Опубликована: Янв. 2, 2025
Abstract Rampant phospholipid peroxidation initiated by iron causes ferroptosis unless this is restrained cellular defences. Ferroptosis increasingly implicated in a host of diseases, and unlike other cell death programs the physiological initiation conceived to occur not an endogenous executioner, but withdrawal guardians that otherwise constantly oppose induction. Here, we profile key ferroptotic defence strategies including regulation, modulation enzymes metabolite systems: glutathione reductase (GR), suppressor protein 1 (FSP1), NAD(P)H Quinone Dehydrogenase (NQO1), Dihydrofolate (DHFR), retinal reductases dehydrogenases (RDH) thioredoxin (TR). A common thread uniting all metabolites combat lipid during dependence on reductant, nicotinamide adenine dinucleotide phosphate (NADPH). We will outline how cells control central carbon metabolism produce NADPH necessary precursors defend against ferroptosis. Subsequently discuss evidence for dysregulation different disease contexts glucose-6-phosphate dehydrogenase deficiency, cancer neurodegeneration. Finally, several anti-ferroptosis therapeutic spanning use radical trapping agents, dependent redox support highlight current landscape clinical trials focusing
Язык: Английский
Процитировано
2
The Science of The Total Environment, Год журнала: 2023, Номер 905, С. 167043 - 167043
Опубликована: Сен. 17, 2023
Язык: Английский
Процитировано
34
Phytomedicine, Год журнала: 2024, Номер 129, С. 155597 - 155597
Опубликована: Апрель 21, 2024
Язык: Английский
Процитировано
5
Frontiers in Pharmacology, Год журнала: 2025, Номер 16
Опубликована: Март 21, 2025
Drug-induced liver injury (DILI) results from the toxicity caused by drugs or their metabolites. Gallic acid (GA) is a naturally occurring secondary metabolite found in many fruits, plants, and nuts. Recently, GA has drawn increasing attention due to its potent pharmacological properties, particularly anti-inflammatory antioxidant capabilities. To best of our knowledge, this first review focus on properties related molecular activation mechanisms regarding protection against hepatotoxicity. We also provide thorough explanation physicochemical fruit sources, toxicity, pharmacokinetics after reviewing substantial number studies. Pharmacokinetic studies have shown that quickly absorbed eliminated when taken orally, which restricts use development. However, bioavailability can be increased optimizing structure changing form administration. Notably, according toxicology conducted range animals clinical trials, rarely exhibits side effects. The antioxidation mainly involved Nrf2, while MAPKs NF-κB signaling pathways. Owing marked prospective candidate for management diverse xenobiotic-induced discuss applications cutting-edge technologies (nano-delivery systems, network pharmacology, organoids) DILI. In addition guiding future research development as medicine, study offers theoretical foundation application.
Язык: Английский
Процитировано
0
Environmental Research, Год журнала: 2024, Номер 252, С. 119113 - 119113
Опубликована: Май 8, 2024
Язык: Английский
Процитировано
4
Biology, Год журнала: 2025, Номер 14(1), С. 81 - 81
Опубликована: Янв. 16, 2025
Iron is a trace element that indispensable for the growth and development of animals. Excessive iron supplementation may lead to overload elevated reactive oxygen species (ROS) production in animals, causing cellular damage. Nevertheless, precise mechanism by which causes cell injury remains be fully elucidated. In this study, 16 male SD rats aged 6 7 weeks were randomly assigned either control group (CON) or an (IO). Rats received 150 mg/kg dextran injections every three days duration four weeks. The results indicated treatment with significantly increased scores steatosis (p < 0.05) inflammation NAS score. integrated transcriptomic proteomic analysis suggests HO-1 Lnc286.2 are potentially significant overload-induced liver rats. vitro experiments utilizing ferric ammonium citrate (FAC) conducted establish model rat liver-derived BRL-3A cells. result found FAC can increase cell’s Fe2+ content 0.05), ROS 0.01), lipid 0.01) levels, expression gene protein aligning findings. inhibition decrease vitality promote thus aggravating FAC-induced Using agonist cobalt protoporphyrin (CoPP) induce overexpression alleviate viability 0.01). addition, siLnc286.2 expression, decline activity, content. conclusion, findings study suggest suppressing Lnc286.2, we enhance HO-1, turn alleviates peroxidation cells increases their antioxidant capacity, thereby exerting protective effect against induced overload.
Язык: Английский
Процитировано
0
Scientific Reports, Год журнала: 2025, Номер 15(1)
Опубликована: Янв. 20, 2025
Язык: Английский
Процитировано
0
Nutrients, Год журнала: 2025, Номер 17(3), С. 547 - 547
Опубликована: Янв. 31, 2025
Background: Ferroptosis is a regulated cell death process linked to various diseases. This study explored whether Epigallocatechin-3-gallate (EGCG), tea-derived antioxidant, could regulate ferroptosis alleviate dextran sulfate sodium (DSS)-induced colitis. Methods: A DSS-induced colitis model was used assess EGCG’s effects. markers, oxidative stress, and iron metabolism were evaluated, alongside Nrf2-GPX4 pathway activation ferritin (FTH/L) expression. Results: Iron dysregulation stress contributed by activating in colonic epithelial cells. EGCG supplementation inhibited ferroptosis, reducing damage. Mechanistically, activated the pathway, enhancing antioxidant defense, improved upregulating Conclusions: effectively suppressed colitis, highlighting its potential as inhibitor therapeutic agent.
Язык: Английский
Процитировано
0
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0