The activation of hepatic stellate cells in non-alcoholic steatosis hepatitis rats by osteopontin antibody

Non-alcoholic steatosis hepatitis (NASH) is one important step in the progression of non-alcoholic fatty liver disease (NAFLD), with the activation of hepatic stellate cells (HSCs) as its key mediator for liver fibrosis. Osteopontin (OPN) is closely related with fibrosis and is important for cell adhesion, migration, proliferation and rearrangement of cytoskeleton. This study thus observed OPN expression in NASH model rats and its correlation with smooth muscle actin (alpha-SMA), in order to investigate the relationship between OPN and HSC activation. NASH model rats were fed with high-fat diet. RT-PCR and Western blotting methods were used to detect gene expression of OPN in liver tissues. Anti-OPN antibody was injected via tail veins. Liver function indexes including ALT, AST, ALP and GCT were tested, along with alpha-SMA gene expression. Immunohistochemistry was employed to detect the positive expression of alpha-SMA. HE and Masson staining were used to observe pathological conditions of liver tissues. OPN gene expression was gradually increased with elongated time (P<0.001). Model rats had significantly elevated serum ALT, AST, ALP and GCT levels (P<0.05). After OPN antibody injection, liver function was improved. NASH rats had elevated alpha-SMA expression, which was down-regulated by OPN antibody. HE and Masson staining showed disrupted liver morphology and fibrosis, which can be partially improved by OPN antibody. High-fat diet induced liver OPN over-expression, which was closely related with NASH. OPN antibody can decreased alpha-SMA expression and inhibit liver fibrosis by inhibiting HSF activation.