LACC1 contributes to inflammation and cognitive disorder after stroke via the AMPK/NLRP3 pathway.
Acta Neurobiol Exp (Wars)
; 82(2): 207-212, 2022.
Article
en En
| MEDLINE
| ID: mdl-35833820
ABSTRACT
The current study aimed to investigate the effects of LACC1 on cognitive disorder due to stroke, as well as its underlying mechanism. LACC1 promoted inflammation and aggravated cognitive impairment in a mouse model of stroke. In an in vitro model of stroke, inhibition of LACC1 reduced inflammation and ROSinduced oxidative stress by activating AMPactivated protein kinase (AMPK) expression and suppressing NLPR3 expression. Furthermore, our studies revealed that inhibition of AMPK activity reduced the effects of siLACC1 on cognitive disorder in mice after stroke via the AMPK/NLPR3 pathway. AMPK activation also reduced the effects of LACC1 on inflammation and ROSinduced oxidative stress via the NLPR3 pathway in the in vitro model that we evaluated. Our study suggests that LACC1aggravated inflammation causes cognitive impairment after stroke via the AMPK/NLRP3 pathway, which may provide a new therapeutic target for stroke and other neurological diseases and their associated complications. In sum, we identified an important role and regulatory mechanism for LACC1 in maintaining strokeinduced cognitive disorder via the AMPK/NLRP3 pathway.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Trastornos del Conocimiento
/
Accidente Cerebrovascular
/
Péptidos y Proteínas de Señalización Intracelular
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Proteínas Quinasas Activadas por AMP
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Proteína con Dominio Pirina 3 de la Familia NLR
/
Inflamación
Tipo de estudio:
Etiology_studies
Límite:
Animals
Idioma:
En
Año:
2022
Tipo del documento:
Article