Diosgenin upregulates axonal guidance partner molecules, Galectin-1 and Secernin-1.
Autor: | Yang X; Section of Neuromedical Science, Institute of Natural Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan., Tohda C; Section of Neuromedical Science, Institute of Natural Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan. Electronic address: chihiro@inm.u-toyama.ac.jp. |
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Jazyk: | angličtina |
Zdroj: | Neuroscience letters [Neurosci Lett] 2024 Nov 01; Vol. 842, pp. 137954. Date of Electronic Publication: 2024 Aug 28. |
DOI: | 10.1016/j.neulet.2024.137954 |
Abstrakt: | Galectin-1, a β-galactosides-binding protein, is widely expressed in various tissues and exhibits diverse biological activities. We previously obtained following findings; 1) Diosgenin, a steroid sapogenin, promoted axonal regeneration in the brain and recovered memory deficits in a model of Alzheimer's disease (AD), 5XFAD mouse; 2) Neuron-specific overexpression of Galectin-1 protein in the hippocampus recovered memory impairment and promoted axonal regeneration in the brain in 5XFAD mice; 3) Secernin-1, a counterpart and axonal guidance molecule for Galectin-1-expressing axons, was secreted from the prefrontal cortical neurons to promote axonal guidance from the hippocampus to the prefrontal cortex. However, it has never been elucidated that diosgenin signaling increase Galectin-1 and Secernin-1 or not. Here, we found that diosgenin treatment upregulated the protein level of Galectin-1 in the hippocampus both in primary cultured neurons and in 5XFAD mouse brains. In addition, diosgenin-induced upregulation of Galectin-1 was diminished by treatment of a neutralizing antibody of 1,25D 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 © 2024 The Authors. Published by Elsevier B.V. All rights reserved.) |
Databáze: | MEDLINE |
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