Ellagic acid improves muscle dysfunction in cuprizone-induced demyelinated mice via mitochondrial Sirt3 regulation.

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  • Additional Information
    • Source:
      Publisher: Elsevier Country of Publication: Netherlands NLM ID: 0375521 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-0631 (Electronic) Linking ISSN: 00243205 NLM ISO Abbreviation: Life Sci Subsets: MEDLINE
    • Publication Information:
      Publication: <2008->: Amsterdam : Elsevier
      Original Publication: Oxford; Elmsford, N. Y. [etc.] Pergamon Press.
    • Subject Terms:
      Behavior, Animal/*drug effects ; Cuprizone/*toxicity ; Demyelinating Diseases/*drug therapy ; Ellagic Acid/*pharmacology ; Mitochondria, Muscle/*drug effects ; Muscular Diseases/*prevention & control ; Sirtuin 3/*metabolism; Animals ; Chelating Agents/toxicity ; Demyelinating Diseases/chemically induced ; Demyelinating Diseases/metabolism ; Demyelinating Diseases/pathology ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria, Muscle/metabolism ; Mitochondria, Muscle/pathology ; Oxidative Stress/drug effects
    • Abstract:
      Sirt3 enzyme and mitochondrial abnormality can be related to excess fatigue or muscular dysfunction in multiple sclerosis (MS).Ellagic acid (EA) has a mitochondrial protector, iron chelator, antioxidant, and axon regenerator in neurons.In this study the effect of EAon muscle dysfunction, its mitochondria, and Sirt3 enzyme incuprizone-induced model of MSwas examined. Demyelination was induced by a diet containing 0.2% w/w cuprizone (Cup) for 42 days and EA administered daily (5, 50, and 100 mg/kg P.O) either with or without cuprizone in mice. Behavioral tests were assessed, and muscle tissue markers ofoxidative stress, mitochondrial parameters, mitochondrial respiratory chain activity, the Sirt3 protein level, and Sirt3 expression were also determined. Luxol fast blue staining and the behavioral tests were performed toassess the implemented model. In Cup group an increased oxidative stress in their muscle tissues was observed. Also, muscle mitochondria exhibited mitochondria dysfunction, lowered mitochondrial respiratory chain activity, Sirt3 protein level, and Sirt3 expression.EA prevented most of these anomalous alterations. Sub-chronicEA co-treatment dose-dependently ameliorated behavioral and muscular impairment in mice that received Cup.EA can effectively protect muscle tissue against cuprizone-induced demeylination via the mitochondrial protection, oxidative stress prevention and Sirt3 overexpression.
      (Copyright © 2019. Published by Elsevier Inc.)
    • Contributed Indexing:
      Keywords: Cuprizone; Ellagic acid; Mitochondrial dysfunction; Multiple sclerosis; Sirt3 enzyme
    • Accession Number:
      0 (Chelating Agents)
      0 (Sirt3 protein, mouse)
      19YRN3ZS9P (Ellagic Acid)
      5N16U7E0AO (Cuprizone)
      EC 3.5.1.- (Sirtuin 3)
    • Publication Date:
      Date Created: 20191015 Date Completed: 20191125 Latest Revision: 20191125
    • Publication Date:
      20221213
    • Accession Number:
      10.1016/j.lfs.2019.116954
    • Accession Number:
      31610192