Bibliographic Details
| Title: |
Antrodia camphorata-Derived Antrodin C Inhibits Liver Fibrosis by Blocking TGF-Beta and PDGF Signaling Pathways |
| Authors: |
Xin-Yi Xu, Yan Geng, Hao-Xiang Xu, Yilin Ren, Deng-Yang Liu, Yong Mao |
| Source: |
Frontiers in Molecular Biosciences, Vol 9 (2022) |
| Publisher Information: |
Frontiers Media S.A., 2022. |
| Publication Year: |
2022 |
| Collection: |
LCC:Biology (General) |
| Subject Terms: |
liver disease, cell migration, hepatic stellate cells, extracellular matrix, cell signaling, Biology (General), QH301-705.5 |
| More Details: |
Hepatic stellate cells (HSCs) play an essential role in the development of liver fibrosis. Antrodia camphorata (A. camphorata) is a medicinal fungus with hepatoprotective effect. This study investigated whether Antrodin C, an A. camphorata-fermented metabolite, could exert a protective role on liver fibrosis both in vitro and in vivo. The anti-fibrotic effect of Antrodin C was investigated in CFSC-8B cell (hepatic stellate cell) stimulated by transforming growth factor-β1 (TGF-β1) or platelet-derived growth factor-BB (PDGF-BB) in vitro and in CCl4 induced liver fibrosis in mice. Antrodin C (50 μM) inhibited TGF-β1 or PDGF-BB stimulated CFSC-8B cell activation, migration and extracellular matrix (ECM) accumulation (all p < 0.05). Antrodin C (3, 6 mg/kg/d) oral administration reduced the degree of liver fibrosis induced by CCl4 in mice. Antrodin C down-regulated the expression of α-smooth muscle actin (α-SMA) and collagen I in fibrotic livers. Furthermore, Antrodin C ameliorated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) elevation in serum (all p < 0.05). Mechanistically, Antrodin C executes its anti-fibrotic activity through negatively modulate TGF-β1 downstream SMAD Family Member 2 (Smad2), AKT Serine/Threonine Kinase 1 (AKT), extracellular signal-regulated kinase (ERK), and P38 MAP Kinase (P38), as well as PDGF-BB downstream AKT and ERK signaling pathways. Antrodin C ameliorates the activation, migration, ECM production in HSCs and CCl4-induced liver fibrosis in mice, suggesting that Antrodin C could serve as a protective molecule against liver fibrosis. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
2296-889X |
| Relation: |
https://www.frontiersin.org/articles/10.3389/fmolb.2022.835508/full; https://doaj.org/toc/2296-889X |
| DOI: |
10.3389/fmolb.2022.835508 |
| Access URL: |
https://doaj.org/article/807ebfee6cca4d22adce13e8417a551f |
| Accession Number: |
edsdoj.807ebfee6cca4d22adce13e8417a551f |
| Database: |
Directory of Open Access Journals |
