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Edaravone Attenuates Disease Severity of Experimental Auto-Immune Encephalomyelitis and Increases Gene Expression of Nrf2 and HO-1
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SYSNO ASEP 0558833 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Edaravone Attenuates Disease Severity of Experimental Auto-Immune Encephalomyelitis and Increases Gene Expression of Nrf2 and HO-1 Tvůrce(i) Michaličková, D. (CZ)
Kubra Ozturk, H. (CZ)
Hroudová, J. (CZ)
Lupták, M. (CZ)
Kučera, T. (CZ)
Hrnčíř, Tomáš (MBU-M) RID, ORCID
Kutinová Canová, N. (CZ)
Šíma, M. (CZ)
Slanař, O. (CZ)Zdroj.dok. Physiological Research. - : Fyziologický ústav AV ČR, v. v. i. - ISSN 0862-8408
Roč. 71, č. 1 (2022), s. 147-157Poč.str. 11 s. Jazyk dok. eng - angličtina Země vyd. CZ - Česká republika Klíč. slova multiple-sclerosis ; active induction ; model ; neurodegeneration ; Experimental autoimmune encephalomyelitis ; Edaravone ; Mitochondrial dysfunction ; Nrf2/HO-1 pathway ; Oxidative stress Vědní obor RIV ED - Fyziologie Obor OECD Physiology (including cytology) CEP GA17-07332S GA ČR - Grantová agentura ČR GA20-09732S GA ČR - Grantová agentura ČR Způsob publikování Open access Institucionální podpora MBU-M - RVO:61388971 UT WOS 000811511400013 EID SCOPUS 85128000650 DOI 10.33549/physiolres.934800 Anotace 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. Pracoviště Mikrobiologický ústav Kontakt Eliška Spurná, eliska.spurna@biomed.cas.cz, Tel.: 241 062 231 Rok sběru 2023 Elektronická adresa https://www.biomed.cas.cz/physiolres/pdf/2022/71_147.pdf
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