Effect of prothymosin α on neuroplasticity following cerebral ischemiareperfusion injury.
Mol Med Rep
; 29(4)2024 04.
Article
en En
| MEDLINE
| ID: mdl-38391118
ABSTRACT
Prothymosin α (ProT), a highly acidic nuclear protein with multiple cellular functions, has shown potential neuroprotective properties attributed to its antinecrotic and antiapoptotic activities. The present study aimed to investigate the beneficial effect of ProT on neuroplasticity after ischemiareperfusion injury and elucidate its underlying mechanism of action. Primary cortical neurons were either treated with ProT or overexpressing ProT by gene transfection and exposed to oxygenglucose deprivation for 2 h in vitro. Immunofluorescence staining for ProT and MAP2 was performed to quantify ProT protein expression and assess neuronal arborization. Mice treated with vehicle or ProT (100 µg/kg) and ProT overexpression in transgenic mice received middle cerebral artery occlusion for 50 min to evaluate the effect of ProT on neuroplasticityassociated protein following ischemiareperfusion injury. The results demonstrated that in cultured neurons ProT significantly increased neurite lengths and the number of branches, accompanied by an upregulation mRNA level of brainderived neurotrophic factor. Furthermore, ProT administration improved the protein expressions of synaptosomalassociated protein, 25 kDa and postsynaptic density protein 95 after ischemicreperfusion injury in vivo. These findings suggested that ProT can potentially induce neuroplasticity effects following ischemiareperfusion injury.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Timosina
/
Daño por Reperfusión
Límite:
Animals
Idioma:
En
Revista:
Mol Med Rep
Año:
2024
Tipo del documento:
Article