Byakangelicin protects against carbon tetrachloride-induced liver injury and fibrosis in mice.
Animals
Apoptosis
/ drug effects
Biopsy
Carbon Tetrachloride
/ adverse effects
Cells, Cultured
Chemical and Drug Induced Liver Injury
/ etiology
Cytokines
/ metabolism
Disease Models, Animal
Furocoumarins
/ pharmacology
Hepatic Stellate Cells
/ drug effects
Hepatocytes
/ drug effects
Liver Cirrhosis
/ etiology
Male
Mice
Protective Agents
/ pharmacology
Signal Transduction
/ drug effects
Smad3 Protein
/ metabolism
Transforming Growth Factor beta
/ metabolism
PDGF
TGF-β
apoptosis
byakangelicin
hepatic stellate cells
liver fibrosis
liver injury
Journal
Journal of cellular and molecular medicine
ISSN: 1582-4934
Titre abrégé: J Cell Mol Med
Pays: England
ID NLM: 101083777
Informations de publication
Date de publication:
08 2020
08 2020
Historique:
received:
09
01
2020
revised:
14
05
2020
accepted:
24
05
2020
pubmed:
10
7
2020
medline:
14
5
2021
entrez:
10
7
2020
Statut:
ppublish
Résumé
Liver fibrosis is a disease caused by long-term damage that is related to a number of factors. The current research on the treatment of liver fibrosis mainly focuses on the activation of hepatic stellate cell, in addition to protecting liver cells. byakangelicin has certain anti-inflammatory ability, but its effect on liver fibrosis is unclear. This study aims to explore whether byakangelicin plays a role in the development of liver fibrosis and to explore its mechanism. We determined that byakangelicin has a certain ability to resist fibrosis and reduce liver cell damage in a model of carbon tetrachloride-induced liver fibrosis in mice. Thereafter, we performed further verification in vitro. The signalling pathways of two important pro-fibrotic cytokines, transforming growth factor-β and platelet-derived growth factor, were studied. Results showed that byakangelicin can inhibit related pathways. According to the hepatoprotective effect of byakangelicin observed in animal experiments, we studied the effect of byakangelicin on 4-HNE-induced hepatocyte (HepG2) apoptosis and explored its related pathways. The results showed that byakangelicin could attenuate 4-HNE-induced hepatocyte apoptosis via inhibiting ASK-1/JNK signalling. In conclusion, byakangelicin could improve carbon tetrachloride-induced liver fibrosis and liver injury by inhibiting hepatic stellate cell proliferation and activation and suppressing hepatocyte apoptosis.
Identifiants
pubmed: 32643868
doi: 10.1111/jcmm.15493
pmc: PMC7412405
doi:
Substances chimiques
Cytokines
0
Furocoumarins
0
Protective Agents
0
Smad3 Protein
0
Transforming Growth Factor beta
0
9-(2,3-dihydroxy-3-methylbutoxy)-4-methoxy-7H-furo(3,2-g)(1)benzopyran-7-one
482-25-7
Carbon Tetrachloride
CL2T97X0V0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
8623-8635Informations de copyright
© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
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