Cerebral neurotoxicity of amino-modified polystyrene nanoplastics in mice and the protective effects of functional food Camellia pollen.
Sci Total Environ
; 912: 169511, 2024 Feb 20.
Article
en En
| MEDLINE
| ID: mdl-38145676
ABSTRACT
Accumulating evidence suggests that nanoplastics contribute to an increased risk of brain damage, however, the precise underlying mechanisms remain unclear. Here, we subjected mice to long-term exposure to amino-modified polystyrene nanoplastics (APS-NPs). These nanoplastics were detected in the mouse brain; coupled with the observed upregulation of Alzheimer's disease-associated genes (APP and MAPT). To further explore nanoplastic damage mechanisms and the corresponding protective strategies against these mechanisms in vitro, we used hCMEC/D3 and HT22 cells. Results showed that APS-NPs disrupted tight junction proteins (Occludin and ZO-1) via TLR2/MMP9 axis, resulting in blood-brain barrier permeation; this was significantly mitigated by functional food Camellia pollen treatment. APS-NPs initiated iNOS and nNOS upregulation within neurons resulting in Sirtuin 1 deacetylase inactivation and CBP acetyltransferase stimulation, ultimately leading to Ac-Tau formation. This process was attenuated by Camellia pollen, which also ameliorated the APS-NPs-induced neuronal apoptosis mediated by the p53/Bax/Bcl-2 axis. Network pharmacology analysis of Camellia pollen offered a further theoretical understanding of its potential applications in preventing and treating nervous system disorders, such as Alzheimer's disease. This study established that Camellia pollen protects the brain against APS-NPs-mediated blood-brain barrier damage and alleviates neuronal apoptosis and Alzheimer's disease-like neurotoxicity. This study elucidates the mechanisms underlying polystyrene-induced brain damage and can be used to inform future prevention and treatment strategies.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Lesiones Encefálicas
/
Camellia
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Nanopartículas
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Enfermedad de Alzheimer
Límite:
Animals
Idioma:
En
Revista:
Sci Total Environ
Año:
2024
Tipo del documento:
Article
País de afiliación:
China