Dataset Information
Apigenin Alleviates Liver Fibrosis by Inhibiting Hepatic Stellate Cell Activation and Autophagy via TGF-?1/Smad3 and p38/PPAR? Pathways.
Ontology highlight
ABSTRACT: Objective
The aim of this study is to confirm the hepatocellular protective functions of apigenin and the molecular mechanism on liver fibrosis in mice.Methods
Carbon tetrachloride (CCl4) and bile duct ligature (BDL) mouse fibrosis models were used to investigate the effects of apigenin on liver fibrosis. Sixty-six male C57 mice were randomly divided into eight groups, including the vehicle group, CCl4 group, CCl4+L-apigenin (20?mg/kg) group, CCl4+H-apigenin (40?mg/kg) group, sham group, BDL group, BDL+L-apigenin(20?mg/kg) group, and BDL+H-apigenin(40?mg/kg) group. Serum liver enzymes (ALT and AST), proteins associated with autophagy, and indicators linked with the TGF-?1/Smad3 and p38/PPAR? pathways were detected using qRT-PCR, immunohistochemical staining, and western blotting.Results
Our findings confirmed that apigenin could decrease the levels of ALT and AST, suppress the generation of ECM, inhibit the activation of HSCs, regulate the balance of MMP2 and TIMP1, reduce the expression of autophagy-linked protein, and restrain the TGF-?1/Smad3 and p38/PPAR? pathways.Conclusion
Apigenin could alleviate liver fibrosis by inhibiting hepatic stellate cell activation and autophagy via TGF-?1/Smad3 and p38/PPAR? pathways.
SUBMITTER: Ji J
PROVIDER: S-EPMC7861947 | biostudies-literature | 2021
REPOSITORIES: biostudies-literature
Publications
Apigenin Alleviates Liver Fibrosis by Inhibiting Hepatic Stellate Cell Activation and Autophagy via TGF-<i>β</i>1/Smad3 and p38/PPAR<i>α</i> Pathways.
PPAR research 20210128
<h4>Objective</h4>The aim of this study is to confirm the hepatocellular protective functions of apigenin and the molecular mechanism on liver fibrosis in mice.<h4>Methods</h4>Carbon tetrachloride (CCl<sub>4</sub>) and bile duct ligature (BDL) mouse fibrosis models were used to investigate the effects of apigenin on liver fibrosis. Sixty-six male C57 mice were randomly divided into eight groups, including the vehicle group, CCl<sub>4</sub> group, CCl<sub>4</sub>+L-apigenin (20 mg/kg) group, CCl< ...[more]
