Objective: To explore the mechanism of edaravone in the treatment of oxidative stress in rats with cerebral infarction based on quantitative proteomics technology.
Method: The modified Zea Longa intracavitary suture blocking method was utilized to make rat CI model. After modeling, the rat was intragastrically given edaravone for 7 days, once a day. After the 7-day intervention, the total proteins of serum were extracted. After proteomics analysis, the differentially expressed proteins are analyzed by bioinformatics. Then chemoinformatics methods were used to explore the biomolecular network of edaravone intervention in CI.
Result: The neurological scores and pathological changes of rats were improved after the intervention of edaravone. Proteomics analysis showed that in the model/sham operation group, 90 proteins in comparison group were upregulated, and 26 proteins were downregulated. In the edaravone/model group, 21 proteins were upregulated, and 41 proteins were downregulated. Bioinformatics analysis and chemoinformatics analysis also show that edaravone is related to platelet activation and aggregation, oxidative stress, intercellular adhesion, glycolysis and gluconeogenesis, iron metabolism, hypoxia, inflammatory chemokines, their mediated signal transduction, and so on.
Conclusion: The therapeutic mechanism of edaravone in the treatment of CI may involve platelet activation and aggregation, oxidative stress, intercellular adhesion, glycolysis and gluconeogenesis, iron metabolism, hypoxia, and so on. This study revealed the serum protein profile of edaravone in the treatment of cerebral infarction rats through serum TMT proteomics and discovered the relevant mechanism of edaravone regulating iron metabolism in cerebral infarction, which provides new ideas for the study of edaravone intervention in cerebral infarction and also provides reference information for future research on the mechanism of edaravone intervention in iron metabolism-related diseases.
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http://dx.doi.org/10.1155/2022/8653697 | DOI Listing |
NPJ Biofilms Microbiomes
December 2024
Costerton Biofilm Center, Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, 2200, Denmark.
The evolution of antimicrobial resistance (AMR) in biofilms, driven by mechanisms like oxidative stress, is a major challenge. This study investigates whether antioxidants (AOs) such as N-acetyl-cysteine (NAC) and Edaravone (ED) can reduce AMR in Pseudomonas aeruginosa biofilms exposed to sub-inhibitory concentrations of ciprofloxacin (CIP). In vitro experimental evolution studies were conducted using flow cells and glass beads biofilm models.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
December 2024
Neuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Eur J Pharmacol
January 2025
Department of Biotechnology, Indian Institute of Technology Hyderabad, Kandi, Sangareddy, Telangana, 502284, India. Electronic address:
Neurodegenerative disorders are characterized by a progressive decline of specific neuronal populations in the brain and spinal cord, typically containing aggregates of one or more proteins. They can result in behavioral alterations, memory loss and a decline in cognitive and motor abilities. Various pathways and mechanisms have been outlined for the potential treatment of these diseases, where redox regulation is considered as one of the most common druggable targets.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Research Center of Basic Integrative Medicine, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, China; Department of Medical Biotechnology, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, China; Dongguan Institute of Guangzhou University of Chinese Medicine, Dongguan, 523808, China. Electronic address:
Background: Brachial plexu root avulsion (BPRA) commonly causes extensive motoneuron death, motor axon degeneration and denervation of biceps, leading to devastating motor dysfunction in the upper limb. Edaravone (Eda) has been proven to exert anti-oxidative and neuroprotective effects on various neurological disorders. Herein, we aimed to investigate the efficacy profile and potential mechanisms of Eda on BPRA in vitro and in vivo models.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
November 2024
Department of Urology, Ningbo Urology and Nephrology Hospital, No.998 Qianhe North Road, Ningbo, 315100, Zhejiang, China.
Edaravone (EDA) has been found to exert protective effects on kidney injury. Nevertheless, the functions of EDA in kidney stones as well as the potential mechanism are vague. Calcium oxalate (CaOx) was used to induce kidney stones cell model with human renal tubular epithelial cell line HK-2.
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