2,4-Dinitrophenol does not exert neuro-regenerative potential in experimental autoimmune neuritis.

Autor: Kohle F; Department of Neurology, Faculty of Medicine, University of Cologne and University Hospital Cologne, Cologne, Germany. Electronic address: felix.kohle@uk-koeln.de., Ackfeld R; Department of Neurology, Faculty of Medicine, University of Cologne and University Hospital Cologne, Cologne, Germany., Klein I; Department of Neurology, Faculty of Medicine, University of Cologne and University Hospital Cologne, Cologne, Germany., Svačina MKR; Department of Neurology, Faculty of Medicine, University of Cologne and University Hospital Cologne, Cologne, Germany., Schneider C; Department of Neurology, Faculty of Medicine, University of Cologne and University Hospital Cologne, Cologne, Germany., van Beers T; Department of Molecular Cell Biology, Institute I for Anatomy, Faculty of Medicine, University Hospital Cologne and University of Cologne, Cologne, Germany., Grandoch A; Department for Oral and Craniomaxillofacial and Plastic Surgery, Faculty of Medicine, University of Cologne and University Hospital of Cologne, Cologne, Germany., Fink GR; Department of Neurology, Faculty of Medicine, University of Cologne and University Hospital Cologne, Cologne, Germany; Cognitive Neuroscience, Research Center Juelich, Institute of Neuroscience and Medicine (INM-3), Juelich, Germany., Lehmann HC; Department of Neurology, Hospital Leverkusen, Leverkusen, Germany., Barham M; Department II of Anatomy, Faculty of Medicine, University of Cologne and University Hospital of Cologne, Cologne, Germany.
Jazyk: angličtina
Zdroj: Neuroscience letters [Neurosci Lett] 2023 Sep 25; Vol. 814, pp. 137456. Date of Electronic Publication: 2023 Aug 28.
DOI: 10.1016/j.neulet.2023.137456
Abstrakt: Objective: We evaluated the potential neuro-regenerative effects of the mitochondrial uncoupler 2,4-Dinitrophenol in experimental autoimmune neuritis, an animal model for an acute autoimmune neuropathy.
Methods: Experimental autoimmune neuritis was induced in Lewis rats. Different concentrations of 2,4-Dinitrophenol (1 mg/kg, 0.1 mg/kg and 0.01 mg/kg) were applied during the recovery phase of the neuritis (at days 18, 22 and 26) and compared to the vehicle. Any effects were assessed through functional, electrophysiological, and morphological analysis via electron microscopy of all groups at day 30. Additional immune-histochemical analysis of inflammation markers and remyelination of the sciatic nerves were performed for the dosage of 1 mg/kg and control.
Results: No enhancement of functional or electrophysiological recovery was observed in all 2,4-Dinitrophenol-treated groups. Cellular inflammation markers of T cells (CD3+) were comparable to control, and an increase of macrophages (IbA1+) invasion in the sciatic nerves was observed. Treatment with 2,4-Dinitrophenol reduced axonal swelling in myelinated and unmyelinated fibers with an increased production of brain-derived neurotrophic factor.
Conclusion: Our findings do not support the hypothesis that repurposing of the mitochondrial uncoupler 2,4-Dinitrophenol exerts functionally relevant neuro-regenerative effects in autoimmune neuritis.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2023 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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