Enriched environment treatment promotes neurofunctional recovery by regulating the ALK5/Smad2/3/Gadd45ß signaling pathway in rats with cerebral ischemia /reperfusion injury.
Neurochem Int
; 178: 105806, 2024 Sep.
Article
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| MEDLINE
| ID: mdl-39025366
ABSTRACT
It has been demonstrated that an enriched environment (EE) treatment can alter neuroplasticity in neurodegenerative diseases. However, the role of EE treatment in ischemic stroke remains unclear. Previous findings have revealed that EE treatment can promote cerebral activin-receptor-like-kinase-5 (ALK5) expression after cerebral ischemia/reperfusion (I/R) injury. ALK5 has been identified as a potential mediator of neuroplasticity through its modulation of Smad2/3 and Gadd45ß. Therefore, the aim of this study was to investigate whether EE treatment could promote neurofunctional recovery by regulating the ALK5/Smad2/3/Gadd45ß pathway. The study utilized the rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). The ALK5/Smad2/3/Gadd45ß signaling pathway changes were evaluated using western blotting (WB). Brain injury was assessed by infarct volume and neurobehavioral scores. The effect of EE treatment on neurogenesis was evaluated using Doublecortin (DCX) and Nestin, axonal plasticity with biotinylated dextran amine (BDA) nerve tracing, and dendritic plasticity was assessed using Golgi-Cox staining. EE treatment has been demonstrated to modulate the Smad2/3/Gadd45ß pathway by regulating the expression of ALK5. The protective effects of EE treatment on brain infarct volume, neurological function, newborn neurons, dendritic and axonal plasticity following cerebral I/R injury were counteracted by ALK5 silencing. EE treatment can enhance neurofunctional recovery after cerebral I/R injury, which is achieved by regulating the ALK5/Smad2/3/Gadd45ß signaling pathway to promote neuroplasticity.
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Banco de datos:
MEDLINE
Asunto principal:
Daño por Reperfusión
/
Transducción de Señal
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Ratas Sprague-Dawley
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Proteína Smad2
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Receptor Tipo I de Factor de Crecimiento Transformador beta
Límite:
Animals
Idioma:
En
Revista:
Neurochem Int
Año:
2024
Tipo del documento:
Article