Tyrosine kinase inhibitor BIBF1120 ameliorates inflammation, angiogenesis and fibrosis in CCl₄-induced liver fibrogenesis mouse model.

ABSTRACT: Hepatic fibrosis, a progressive chronic disease mainly caused by hepatitis viral infections, alcohol abuse or metabolic syndrome leading to liver dysfunction and is the growing cause of mortality worldwide. Tyrosine kinase inhibitor BIBF1120 (Nintedanib) has been evaluated in clinical trials for idiopathic pulmonary fibrosis and advanced Hepatocellular carcinoma, but has not been explored for liver fibrosis yet. In this study, we aimed to investigate the therapeutic effects and mechanism of BIBF1120 in liver fibrogenesis. The effects of BIBF1120 were evaluated in TGFβ-activated mouse 3T3 fibroblasts, LX2 cells, primary human hepatic stellate cells (HSCs) and CCl₄-induced liver fibrogenesis mouse model. Fibroblasts-conditioned medium studies were performed to assess the paracrine

SUBMITTER: Ozturk Akcora B 

PROVIDER: S-EPMC5349608 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature