Medium- and long-chain triglyceride propofol activates PI3K/AKT pathway and inhibits non-alcoholic fatty liver disease by inhibiting lipid accumulation.
J Bioenerg Biomembr
; 56(1): 45-53, 2024 Feb.
Article
en En
| MEDLINE
| ID: mdl-38032443
ABSTRACT
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease. The mechanism by which medium- and long-chain triglyceride (MCT/LCT) propofol plays a role in promoting NAFLD remains unclear. In this study, we investigated the effect of MCT/LCT propofol on NAFLD progression and its mechanism of action. In Huh-7 and HepG3 cells induced by free fatty acids (FFA), propofol downregulated the expression levels of TG and lipid metabolism-related proteins by promoting the activation of the PI3K/AKT pathway and suppressing FFA-induced lipid metabolic disorders. In a high-fat diet (HFD) -induced NAFLD mouse model, we demonstrated that propofol significantly inhibited liver steatosis, inflammatory cell infiltration, and fibrosis. In conclusion, our results suggest that MCT/LCT propofol reduces liver lipid accumulation by activating the PI3K/AKT pathway and further suppressing the NAFLD process.
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Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Propofol
/
Enfermedad del Hígado Graso no Alcohólico
Límite:
Animals
Idioma:
En
Año:
2024
Tipo del documento:
Article