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Edaravone Attenuates Disease Severity of Experimental Auto-Immune Encephalomyelitis and Increases Gene Expression of Nrf2 and HO-1

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388971%3A_____%2F22%3A00558833" target="_blank" >RIV/61388971:_____/22:00558833 - isvavai.cz</a>

  • Alternative codes found

    RIV/00064165:_____/22:10445179 RIV/00216208:11110/22:10445179

  • Result on the web

    <a href="https://www.biomed.cas.cz/physiolres/pdf/2022/71_147.pdf" target="_blank" >https://www.biomed.cas.cz/physiolres/pdf/2022/71_147.pdf</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.33549/physiolres.934800" target="_blank" >10.33549/physiolres.934800</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Edaravone Attenuates Disease Severity of Experimental Auto-Immune Encephalomyelitis and Increases Gene Expression of Nrf2 and HO-1

  • Original language description

    The aim of this study was to evaluate therapeutic potential of edaravone in the murine model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE) and to expand the knowledge of its mechanism of action. Edaravone (6 mg/kg/day) was administered intraperitoneally from the onset of clinical symptoms until the end of the experiment (28 days). Disease progression was assessed daily using severity scores. At the peak of the disease, histological analyses, markers of oxidative stress (OS) and parameters of mitochondria! function in the brains and spinal cords (SC) of mice were determined. Gene expression of inducible nitric oxide synthase (iNOS), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and peroxisome proliferator-activated receptor-gamma coactivator (PGC)-'alpha was determined at the end of the experiment. Edaravone treatment ameliorated EAE severity and attenuated inflammation in the SC of the EAE mice, as verified by histological analysis. Moreover, edaravone treatment decreased OS, increased the gene expression of the Nrf2 and HO-1, increased the activity of the mitochondrial complex reduced the activity of the mitochondrial complex IV and preserved ATP production in the SC of the EAE mice. In conclusion, findings in this study provide additional evidence of edaravone potential for the treatment of multiple sclerosis and expand our knowledge of the mechanism of action of edaravone in the EAE model.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30105 - Physiology (including cytology)

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2022

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Physiological Research

  • ISSN

    0862-8408

  • e-ISSN

    1802-9973

  • Volume of the periodical

    71

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    CZ - CZECH REPUBLIC

  • Number of pages

    11

  • Pages from-to

    147-157

  • UT code for WoS article

    000811511400013

  • EID of the result in the Scopus database

    2-s2.0-85128000650