Protective effect of Idelalisib on carbon tetrachloride-induced liver fibrosis via microRNA-124-3P/phosphatidylinositol-3-hydroxykinase signalling pathway.

ABSTRACT: Liver fibrosis is the repair process of abnormal connective tissue hyperplasia after liver damage caused by different causes. Inhibition of PI3K/Akt signalling pathway can reduce the deposition of extracellular matrix, inhibit the proliferation of hepatic stellate cells (HSCs), and promote its apoptosis to achieve the purpose of therapy. This study aimed to investigate the effect of Idelalisib (PI3K inhibitor) on carbon tetrachloride (CCl₄ )-induced liver fibrosis in mice. We used CCl₄ -induced liver fibrosis mouse model in vivo and TGF-β1-stimulated HSCs to evaluate the antifibrosis activity of Idelalisib. In vivo, Idelalisib significantly alleviated CCl₄ -induced liver damage, collagen deposition, and hydroxyproline accumulation in mice. Immunohistochemis

SUBMITTER: Li X 

PROVIDER: S-EPMC8650042 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature