AHCCâ inhibited Hepatic Stellate Cells Activation by Regulation of Cytoglobin induction via TLR2-SAPK/JNK pathway and Collagen Production via TLR4-NFκB pathway.
Am J Physiol Gastrointest Liver Physiol
; 2024 Sep 24.
Article
en En
| MEDLINE
| ID: mdl-39316687
ABSTRACT
[Introduction] Cirrhosis, which represents the end stage of liver fibrosis, remains a life-threatening condition without effective treatment. Therefore, prevention of the progression of liver fibrosis through lifestyle habits such as diet and exercise is crucial. The functional food AHCCâ has been reported to be effective in improving the pathophysiology of various liver diseases. In this study, the aim was to analyze the influence of AHCCâ on hepatic stellate cells, which are responsible for liver fibrosis. [Materials and Methods] Eight-week-old male C57BL6/j mice were induced liver fibrosis by intraperitoneal injection of carbon tetrachloride. Simultaneously, they were orally administered 3% AHCCâto investigate its impact on the progression of liver fibrosis. Using the human hepatic stellate cell line HHSteC, we analyzed the influence of AHCCâ on the expression of molecules related to hepatic stellate cell activation. [Results] The administration of AHCCâ resulted in reduced expression of collagen1a, alpha smooth muscle actin (αSMA), and Heat shock protein 47 in the liver. Furthermore, the expression of cytoglobin, a marker for quiescent hepatic stellate cells, was enhanced. In vitro study, it was confirmed that AHCCâ inhibited αSMA by induction of cytoglobin via upregulating the SAPK/JNK pathway through toll-like receptor (TLR) 2. In addition, AHCCâ suppressed collagen1a production by hepatic stellate cells through TLR4-NFκß pathway. [Conclusion] AHCCâ was suggested to suppress hepatic fibrosis by inhibition of hepatic stellate cells activation. Daily intake of AHCCâ from mild fibrotic stages may have the potential to prevent the progression of liver fibrosis.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Idioma:
En
Revista:
Am J Physiol Gastrointest Liver Physiol
Asunto de la revista:
FISIOLOGIA
/
GASTROENTEROLOGIA
Año:
2024
Tipo del documento:
Article
País de afiliación:
Japón