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Diosgenin upregulates axonal guidance partner molecules, Galectin-1 and Secernin-1
1Section of Neuromedical Science, Institute of Natural Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Neuroscience Letters
|August 30, 2024
Summary
Diosgenin promotes brain repair in Alzheimer
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Galectin-1 is a protein involved in various biological activities.
- Previous studies showed diosgenin and Galectin-1 aid axonal regeneration and memory recovery in Alzheimer's disease (AD) models.
- The mechanism by which diosgenin influences Galectin-1 and Secernin-1 in AD remains unclear.
Purpose of the Study:
- To investigate if diosgenin signaling increases Galectin-1 and Secernin-1 expression.
- To explore the role of the 1,25D3-membrane-associated rapid response steroid-binding receptor (1,25D3-MARRS) in diosgenin's effects.
Main Methods:
- Treated primary cultured neurons and 5XFAD mouse brains with diosgenin.
- Utilized a neutralizing antibody against 1,25D3-MARRS.
- Performed Galectin-1 knockdown in hippocampal neurons.
- Administered diosgenin to 5XFAD mice and analyzed prefrontal cortical neurons.
Main Results:
- Diosgenin upregulated Galectin-1 protein levels in hippocampal neurons and 5XFAD mouse brains.
- The diosgenin-induced increase in Galectin-1 was reduced by anti-1,25D3-MARRS antibody treatment.
- Knocking down Galectin-1 impaired diosgenin's effect on axonal growth.
- Diosgenin administration increased Secernin-1 expression in prefrontal cortical neurons of 5XFAD mice.
Conclusions:
- Diosgenin upregulates Galectin-1 and Secernin-1, potentially via the 1,25D3-MARRS receptor.
- Diosgenin facilitates Galectin-1-Secernin-1-mediated axonal growth.
- Diosgenin shows promise for enhancing brain repair in Alzheimer's disease.
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