Role of PPAR-γ-regulated autophagy in genistein-induced inhibition of hepatic stellate cell activation / 南方医科大学学报
Journal of Southern Medical University
; (12): 561-565, 2019.
Article
en Zh
| WPRIM
| ID: wpr-772043
Biblioteca responsable:
WPRO
ABSTRACT
OBJECTIVE@#To investigate the inhibitory effect of genistein on activation of hepatic stellate cells (HSCs) and the role of the autophagy pathway regulated by PPAR-γ in mediating this effect.@*METHODS@#Cultured HSC-T6 cells were exposed to different concentrations of genistein for 48 h, and HSC activation was verified by detecting the expressions of -SMA and 1(I) collagen; autophagy activation in the cells was determined by detecting the expressions of LC3-II and p62 using Western blotting. The autophagy inhibitor 3-MA was used to confirm the role of autophagy in genistein-induced inhibition of HSC activation. A PPAR-γ inhibitor was used to explore the role of PPAR-γ in activating autophagy in the HSCs.@*RESULTS@#Genistein at concentrations of 5 and 50 μmol/L significantly inhibited the expressions of -SMA and 1(I) collagen ( < 0.05), markedly upregulated the expressions of PPAR-γ and the autophagy-related protein LC3-II ( < 0.05) and significantly down-regulated the expression of the ubiqutin-binding protein p62 ( < 0.05) in HSC-T6 cells. The cells pretreated with 3-MA prior to genistein treatment showed significantly increased protein expressions of -SMA and 1(I) collagen compared with the cells treated with genistein only ( < 0.05). Treatment with the PPAR-γ inhibitor obviously lowered the expression of LC3-II and enhanced the expression p62 in genistein-treated HSC-T6 cells, suggesting the activation of the autophagy pathway.@*CONCLUSIONS@#PPAR-γ- regulated autophagy plays an important role in mediating genistein-induced inhibition of HSC activation .
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Base de datos:
WPRIM
Asunto principal:
Farmacología
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Fisiología
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Autofagia
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Anticarcinógenos
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Genisteína
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Colágeno Tipo I
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PPAR gamma
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Células Estrelladas Hepáticas
Límite:
Humans
Idioma:
Zh
Revista:
Journal of Southern Medical University
Año:
2019
Tipo del documento:
Article