Astragaloside-IV promotes autophagy via the Akt/mTOR pathway to improve cellular lipid deposition.
Medicine (Baltimore)
; 103(16): e37846, 2024 Apr 19.
Article
em En
| MEDLINE
| ID: mdl-38640324
ABSTRACT
The current study aimed to investigate the potential role of astragaloside IV (AS-IV) in improving cellular lipid deposition and its underlying mechanism. A fatty liver cell model was established by treating hepatoma cells with palmitic acid. AS-IV and SC79 were used for treatment. Oil Red O staining was applied to detect intracellular lipid deposition, and transmission electron microscopy was utilized to assess autophagosome formation. Immunofluorescence double staining was applied to determine microtubule-associated proteins 1A/1B light chain 3 (LC3) expression. Western blot analysis was performed to detect the expression of LC3, prostacyclin, Beclin-1, V-akt murine thymoma viral oncogene homolog (Akt), phosphorylated Akt, mTOR, and phosphorylated mTOR. Oil Red O staining revealed that AS-IV reduced intracellular lipid accumulation. Further, it increased autophagosome synthesis and the expression of autophagy proteins LC3 and Beclin-1 in the cells. It also reduced the phosphorylation levels of Akt and mTOR and the levels of prostacyclin. However, the effects of AS-IV decreased with SC79 treatment. In addition, LC3Bâ
+â
BODIPY493/503 fluorescence double staining showed that AS-IV reduced intracellular lipid deposition levels by enhancing autophagy. AS-IV can reduce lipid aggregation in fatty liver cells, which can be related to enhanced hepatocyte autophagy by inhibiting the Akt/mTOR signaling pathway.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Saponinas
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Autofagia
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Triterpenos
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Metabolismo dos Lipídeos
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Fígado Gorduroso
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article