Published: Jan. 1, 2024
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Language: Английский
Published: Jan. 1, 2024
Download This Paper Open PDF in Browser Add to My Library Share: Permalink Using these links will ensure access this page indefinitely Copy URL DOI
Language: Английский
Pesticide Biochemistry and Physiology, Journal Year: 2024, Volume and Issue: 202, P. 105935 - 105935
Published: April 28, 2024
Language: Английский
Citations
6International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 277, P. 134231 - 134231
Published: July 27, 2024
Language: Английский
Citations
5The Science of The Total Environment, Journal Year: 2024, Volume and Issue: 940, P. 173575 - 173575
Published: May 31, 2024
Language: Английский
Citations
4Drug Design Development and Therapy, Journal Year: 2025, Volume and Issue: Volume 19, P. 1271 - 1287
Published: Feb. 1, 2025
This study aimed to investigate the mechanisms and specific targets of cordycepin in treatment renal fibrosis using a unilateral ischemia-reperfusion (UIR) model. A UIR mouse model was established, followed by intraperitoneal injections Mdivi-1. Masson's trichrome staining PAS were used identify tubulointerstitial assess degree injury. Fibrosis markers mitochondrial dynamics-related proteins evaluated Western blotting, while differential gene expression pathway enrichment analyzed RNA-seq. Molecular docking, molecular dynamics simulations surface plasmon resonance conducted validate binding sites on target protein Drp1. Immunofluorescence vitro experiments further elucidated therapeutic mechanism cordycepin. In vivo showed that injection significantly reduced inflammation fibrosis, lowered serum creatinine levels, decreased collagen deposition. Transcriptome analysis revealed downregulated fission upregulated fusion pathway. blotting levels α-SMA FN, as well downregulation Drp1, MFF, Fis1, upregulation OPA1 Mfn2. vitro, inhibited TGF-β-induced injury NRK-52E cells, reducing Drp1 IL-6 secretion. Crosstalk confirmed crucial for anti-fibrotic effects suppressing fibroblast activation. Cordycepin ameliorates targeting inhibit injured tubular epithelial secretion inhibiting
Language: Английский
Citations
0Journal of Agricultural and Food Chemistry, Journal Year: 2025, Volume and Issue: unknown
Published: April 16, 2025
Thiacloprid (THI) is a synthetic insecticide, the misuse targeted chiefly to control aphid pest species in orchards and vegetables. Melatonin (MET) hormone that plays crucial physiological roles anti-inflammatory capacities of fish. We explored function MET (100 μM) mitigate toxicity induced by THI (20 lymphocytes. Our results indicate led notable rise lymphocyte mortality. Lymphocytes exposed exhibited heightened incidence pyroptosis, accompanied upregulation expression associated with pyroptosis (NLRP3, GSDMEA, IL-18). Meanwhile, exposure decrease mitochondrial membrane potential, an increase mtROS levels, reduction intracellular ATP, DNA, NADPH/NADP+ indicating imbalance metabolism within Additionally, these effects were reversed treatment, where MitoQ treatment showed suppression reduced caused via mtROS/cGAS-STING/NF-κB axis. Importantly, provided defense against immunotoxic impacts ameliorating enhancing capability research potentiates safeguarding cultured fish from biological hazards highlights valuable application common carp.
Language: Английский
Citations
0Pesticide Biochemistry and Physiology, Journal Year: 2025, Volume and Issue: unknown, P. 106450 - 106450
Published: May 1, 2025
Language: Английский
Citations
0Journal of Advanced Research, Journal Year: 2024, Volume and Issue: unknown
Published: June 1, 2024
Metabolic inflammation (metaflammation) in obesity is primarily initiated by proinflammatory macrophage infiltration into adipose tissue. SelenoM contributes to the modulation of antioxidative stress and multiple pathological processes; however, its roles metaflammation (M1)-like state tissue have not been determined. We hypothesize that could effectively regulate via Hippo-YAP/TAZ-ROS signaling axis derived from a high-fat diet. Morphological changes were examined hematoxylin-eosin (H&E) staining fluorescence microscopy. The glucose tolerance test (GTT) insulin (ITT) used evaluate impact deficiency on blood levels. RNA-Seq analysis, LC-MS Mass spectrometry analysis western blotting performed detect levels genes proteins related glycolipid metabolism Herein, we evaluated inflammatory features metabolic microenvironment mice with SelenoM-deficient tissues multi-omics analyses. deletion resulted disturbances resistance, thereby accelerating weight gain, adiposity, hyperglycemia. Mice lacking white adipocytes developed severe adipocyte hypertrophy impaired lipolysis. aggravated generation ROS reducing equivalents (NADPH glutathione) adipocytes, promoting cytokine production M1-proinflammatory reaction, which was change nuclear factor kappa-B (NF-κB) macrophages. Mechanistically, promoted Hippo-YAP/TAZ-ROS-mediated transcriptional regulation targeting large tumor suppressor 2 (LATS2). Moreover, supplementation N-acetyl cysteine (NAC) reduce excessive oxidative partially rescued responses M1 activation. Our data indicate ameliorates mainly obesity. identification as key regulator presents opportunities for development novel therapeutic interventions dysfunction
Language: Английский
Citations
3Journal of Environmental Management, Journal Year: 2025, Volume and Issue: 382, P. 125360 - 125360
Published: April 14, 2025
Language: Английский
Citations
0Chemical Research in Toxicology, Journal Year: 2024, Volume and Issue: 37(11), P. 1794 - 1806
Published: Nov. 1, 2024
Mitochondria, pivotal to cellular metabolism, serve as the primary sources of biological energy and are key regulators intracellular calcium ion storage, crucial for maintaining homeostasis. Dysfunction in these organelles impairs ATP synthesis, diminishing functionality. Emerging evidence implicates mitochondrial dysfunction etiology progression diverse diseases. Environmental factors that induce dysregulation raise significant public health concerns, necessitating a nuanced comprehension classification mitochondrial-related hazards. This review systematically adopts toxicological perspective illuminate functions mitochondria, offering comprehensive exploration how toxicants instigate dysfunction. It delves into disruption initiation fragility autophagy, induction mutations DNA by mutagens. The overarching objective is enhance our understanding repercussions damage on human health.
Language: Английский
Citations
2Published: Jan. 1, 2024
Download This Paper Open PDF in Browser Add to My Library Share: Permalink Using these links will ensure access this page indefinitely Copy URL DOI
Language: Английский
Citations
0